Exam 5 Flashcards
1
Q
Intramuscular (IM) Route of Vaccine Administration
A
Upper thigh in infants, deltoid when muscle mass is sufficient ***Buttock should be avoided due to sciatic nerve damageand inconsistent IM deposition
- Hep A & B
- DTap/Dtap
- Hib
- Strep
- IPV
- Influenza
- Meningococcal
- HPV
2
Q
Subcutaneous (SQ)Route of Vaccine Administration
A
Usually “pinch” the skin and inject into fatty tissue under the skin. MMR & Varicella
3
Q
Pneumococcal Conjugate Vaccine (PCV) Types
A
23-valent pneumococcal polysaccharide (23-PS) available (>2 years) FDA licensed new 7-valent pneumococcal conjugate vaccine (PCV7) - < 2 years Prevnar 13 – a 13-valent pneumococcal conjugate vaccine (PCV13)
4
Q
Pneumococcal Conjugate Vaccine (PCV):Contraindications/Precuations
A
- known hypersensitivity
* moderate to severe illness
5
Q
Pneumococcal Conjugate Vaccine (PCV):Side Effects
A
- Local erythema
- Induration
- Tenderness
- Fussiness
- Low grade to moderate fever
6
Q
MMR Vaccine Measles, Mumps, Rubella Administration
A
- Given subcutaneously
- 1st dose: 12-15 months (minimum age is 12 months)
- 2nd dose: 4-6 years (at school entry)
7
Q
MMR Vaccine Measles, Mumps, Rubella Contraindications & Precuations
A
Contraindications:
- Anaphylaxis
- Pregnancy
- Immunodeficiency Precautions:
- Recent immune globulin administration
- History of thrombocytopenia
8
Q
MMR Vaccine Measles, Mumps, Rubella Side Effects:
A
- Local tenderness/swelling
- Fever 7-10 days after
- Morbiliform rash
9
Q
Active Immunity
A
Vaccination with live, live attenuated, or inactivated organisms, their components or their products to stimulate protective immunologic response
10
Q
Contraindications for All Vaccines
A
Anaphylactic reaction to previous doses is an absolute contraindication for further doses Anaphylactic reaction to any component Moderate to severe illness with or without fever
11
Q
Rotavirus Vaccine
A
Pentavalent Rotavirus Vaccine Adminster three primary doses at 2, 4 and 6 months ***Should not be initiated after age 12 weeks and not to be given at all after 32 weeks of age
12
Q
Meningococcal Vaccine - MPSV 4
A
Children age 2-10 in susceptible children
- Complement deficiency
- Anatomic or functional asplenia
- Other high-risk groups
13
Q
Varicella Vaccine: Administration
A
- live, attenuated virus
- 1st dose - 12-18 months or teens and adults with no history of natural infection
- 2nd dose – 4-6 years (new for 2007)95% seroconvert after 1 dose
- > 13 years, 2nd dose 4-8 weeks later
14
Q
Varicella Vaccine: Side Effects
A
- Local tenderness
* varicelliform rash within 1 month
15
Q
Influenza Vaccine Administration
A
- First dose: 6 months
- Dose yearly – vaccine typically updated.
- After age 2, option of live-attenuated (nasal spray).
16
Q
Influenza Vaccine Precautions
A
- Avoid in asthma, wheezing past 12 months, underlying medical conditions.
- Avoid if egg allergy.
17
Q
Injectable Polio Vaccine (IPV) Administration
A
- Given intramuscularly
- 2 months, 4 months, 6-9 months, 4-6 years
- Minimum of 4 weeks between 1st and 2nd doses
18
Q
Injectable Polio Vaccine (IPV) Side Effects
A
- VAPP with OPV
- Hypersensitivity
- Guillan-Barre??
19
Q
Diphtheria, Tetanus and Pertussis Vaccine DTaP, TDaP, Td Administration
A
Diphtheria toxoid;Tetanus toxoid;Acellular pertussis
- Four primary doses and one booster
- Given intramuscularly
- Typically 2, 4, 6 months, and 12-18 months
- Booster at 4-6 years; or if dirty cut and less than 5 year since last booster
20
Q
Diphtheria, Tetanus and Pertussis Vaccine DTaP, TDaP, Td Contraindications & Precuations
A
Contraindications
- Encephalopathy within 7 days of administration of previous dose Precuations
- Temperature >40.5° C within 48 hours of previous dose
- Collapse or shock-like state within 48 hrs of previous dose
- Seizures within 3 days of previous dose
- Persistent/inconsolable crying >3 hours within 48 hrs of previous dose
21
Q
Meningococcal Vaccine - MCV4
A
- Meningococcal Conjugate Vaccine
- Administer at 11-12 yrs or the 7th grade physical
- A booster is given at college entry
22
Q
Recombinant Products Vaccines
A
Hepatitis B Recombinant Products - A preparation of a weakened or killed pathogen, such as a bacterium or virus, or of a portion of the pathogen’s structure that upon administration stimulates antibody production or cellular immunity against the pathogen but is incapable of causing severe infection
23
Q
Immunogenic Components of Bacteria Vaccines
A
Pertussis, Haemophilus influenzae type B, Streptococcus pneumoniae Toxoids – Diphtheria, Tetanus
24
Q
Haemophilus influenzae, type B(Hib) Vaccine
A
Administration:
- Given Intramuscularly
- Can be given with other vaccinations
- 2, 4, and 6 months with booster at 12-15 months No contraindications and minimal side effects.
25
Inactivated/Killed Vaccines
Polio, Hepatitis A, Influenza
26
HPV Vaccine
* Quadrivalent vaccine against HPV Types 6, 11, 16, and 18
* Administer first dose to females/males 11-12 years or before they become sexually active
* Second dose at 2 months
* Third dose at 6 months
27
Passive Immunity
Trans-placental transfer of maternal antibodies Administration of antibodies, either as: Immunoglobulin, OR Monoclonal antibody
28
Heptatis A
* Minimum age is 12 months
* 2 doses, given at least 6 months apart, starting after 1 year of age
* Can be given to older children and adolescents
29
Common Vaccine Side Effects
* Localized tenderness
* Localized erythema
* Fever
* Fussiness
* Allergic reaction
30
Other Ingredients in Vaccine
* Suspending Fluids (saline, tissue culture)
* Preservatives
* Stabilizers
* Antibiotics (Prevent bacterial overgrowth)
* Adjuvants to enhance immunogenicity *All can contribute to local side effects and rarely, can cause anaphylaxis (egg antigens, antibiotics, gelatin)
31
Hepatitis B Vaccine Who gets it:
Universal hep B immunizations in infancy as well as children and adolescents who missed immunization during infancy or those who are at increased risk
32
Hepatitis B Vaccine Administration
Given IM (intramuscularly) 1st dose – at birth (within 12 hours) 2nd dose – 1-2 months 3rd dose – 6 months
33
Hepatitis B Vaccine Contraindications and Side Effects
Contrindications: none SE: Localized tenderness, rare hypersensitivity, reaction to yeast or vaccine preservatives
34
Live attenuated vaccinations
Measles, mumps, rubella, varicella Live Attenuated is the actual viruses – weakened or altered so that the child doesn’t get sick. These vaccines STING!
35
What is responsible for inflammation?
Inflamasome
36
Humoral adaptive or acquired immune system includes:
B Cells, plasma cells, antibody
37
Cellular adaptive or acquired immune system includes:
T cells, macrophages, neutrophils
38
80-90% of all immune responses occur through which branch of the immune system?
Innate
39
Histiocytes are macrophages in the:
Tissue
40
True/False: Mononuclear phagocytes have a role in both adaptive and innate immunity?
True
41
What is the predominant cell making up the white cell count?
Neutrophils
42
True/False: The host produces PAMPs.
False: host does not produce PAMPS so the innate system does not have to discriminate self from non-self.
43
What are PAMPs recognized by?
PRRs
44
PRRs on phagocytes results in: (4)
1) Phagocytosis2) Opsonization through acute phase proteins3) Elevated anti-microbial activity4) Up-regulation of A) adhesion molecules, B) Co-stimulatory molecules
45
What is opsonization?
INDIRECT RECOGNITION through opsonins: Enhanced phagocytosis that is usually mediated by ligands and receptors, that utilizes the process of phagocytosis. THE JELLY ON THE BREAD
46
Eosinophils are important in:
Parasitic infections, allergies
47
Mast cells are important in:
allergies and anaphylaxis: Contain pre-formed histamine
48
Basophils during inflammation release potent _________ that exacerbate the response. The granules stain ______
Mediators, blue
49
_____________ have high nuclear to cytoplasmic ratios and include T-cells, B-cells, and NK cells
Lymphocytes
50
What cells react with tumor cells and virally infected cells and kill them through apoptosis and enzymes?
Natural Killer cells
51
T/F: Acute phase proteins help in opsonization because cells have receptors for these acute phase proteins on their cell surface?
True
52
What is the major coordinator of inflammation and made up of over 20 different proteins?
Complement (Part of Innate Immune system)
53
A group of proteins that have an effect on other cells:
Interferons
54
T/F: Alpha or beta interferons infect adjacent cells?
False: They stop infection of adjacent cells
55
What interferon works through the adaptive immune response to activate T cells and macrophages?
Gamma interferon
56
In acute inflammation you tend to have higher numbers of what cells?
Neutrophils and activated T helper cells
57
In chronic inflammation you tend to have higher numbers of what cells?
Macrophages, t cytotoxic, and B cells
58
A glycoprotein secreted by a plasma cell that is specific for an epitope on an antigen is what?
An antibody
59
Fab is the fraction of _________ ___________ while Fc is fraction of _______________.
antigen binding, crystallization
60
T/F: The TCR is secreted
False- never secreted
61
T/F: T and B memory cells are produced following antigen stimulation?
True
62
The biologically relevant portion of an antibody is what?
Fc (Fraction of crystallization)
63
Antibodies functionality is conferred by: (4)
1) Fc receptors on cells2)Complement activation3) Complement receptors4) Placental transfer
64
T/F: IgM crosses the placenta
False
65
T/F: IgM is a pentamer
TRUE
66
T/F: IgM is first immunoglobulin secreted upon antigen stimulation
True
67
T/F: IgE has an extra piece on the Fc portion that makes it bind only to mast cells
True- In the absence of antigen
68
IgA is found in __________
Secretions
69
Ig__ functions as a marker of maturation
IgD
70
Genetic variability: ________ is conferred by the Fc portion. ____________ is minor genetic differences that are obtained from mom and dad. _______ is an antibody to the antigen combining site (the Vh and Vl)
Isotype, Allotype, Idiotype
71
T/F: If IgM is present in the baby, the baby is responding?
True: If IgG is present, do not know if it is from mom or baby
72
What thyroid hormone is the major product of the thyroid gland?
T4
73
What thyroid hormone is active at the cellular level?
T3biologically more active; shorter half life
74
Primary hypothyroidism affects what level?
Gland
75
Secondary hypothyroidism affects what level?
Pituitary
76
Tertiary hypothryoidism affects what level?
Hypothalamus
77
Describe the hypothalamic-pituitary-thyroid axis:
Hypothalamus releases TRH which stimulates pituitary. Pituitary releases TSH which acts on the thyroid. Thyroid hormones then exhibit NEGATIVE feedback on the pituitary and hypothalamus.
78
Describe the spectrum of presentation of hypothyroidism (3).
1. Subclinical hypothyroidism (elevated TSH, normal T4)2. Symptomatic disease3. Severe myxedema coma
79
Etiologies of Primary Hypothyroidism (9)
1. Autoimmune (Hashimotos)2. Idiopathic3. Post ablation 4. Post external radiation5. Thyroiditis (subacute, silent, postpartum)6. Infiltrative Disease (lymphoma, sacroid, amyloidosis, Tuberculosis)7. Congenital8. Iodine Deficiency9. Drug-induced hypothyroidism (Amiodarone, lithium)
80
Etiologies of Secondary Hypothyroidism (3)
caused by insults to the pituitary gland1. Neoplasm2. Infiltrative3. Hemorrhage into the gland
81
Etiologies of Tertiary Hypothyroidism (4)
1. Neoplasm2. Infiltrative Disease3. Anorexia Nervosa4. Cerebrovascular or surgical insult
82
What causes systemic symptoms of hypothyroidism?
lack of T3
83
Frequent Signs and Symptoms of Hypothyroidism(all of the signs and symptoms are listed)
WeaknessEdema of faceLethargyCourse SkinSlow MovementsEdema of EyelidsSensation of ColdHoarsenessPeripheral EdemaDry SkinDecreased SweatingPallor of LipsSlow speechCold SkinConstipationThick TongueParesthesiasGain in weightMuscle WeaknessSlow cerebration
84
Typical Symptoms of Hypothyroidism (6)
fatigueweaknesscold intoleranceconstipationweight gaindeepening of voice
85
Cutaneous Symptoms of Hypothyroidism (4)
dry, scaly, yellow skinnon-pitting waxy edema of the facemyxedemathinning of eyebrows
86
Cardiac Symptoms (3)
bradycardiaenlarged heartlow voltage electrocardiogram
87
Hypothyroidism Symptoms in the Neck (5)
PainSwellingTendernessNodulesCystsor could be asymptomatic
88
Neurological Symptoms of Hypothyroidism (3)
ParesthesiaAtaxiaProlongation of DTR
89
Describe the hormone levels in HYPOthyroidism - TSH and T4
TSH: increased (normal 0.5-5.0 ug/mL)Free T4: low or low-normal (normal 0.7-1.86 ng/dL)thyroid is unable to produce sufficient quantities of hormone (low T4), so pituitary compensates further stimulating the thyroid (high TSH)
90
What is Hashimoto's Disease? What markers will be present?
Autoimmune thyroiditisPositive test for antibodies - Anti-Tg and Anti-TPO10 x more common in women
91
What is subclinical hypothyroidism? How is it treated?
Elevated TSH with normal free T4TSH > 10: treatTSH 5-10: monitor or possible trial of hormone replacement
92
What is Acquired Transient Central Hypothyroidism also known as Euthyroid Sick Syndrome?
Extremely ill patients with non thyroidal illnessEuthyroid with elevated TSH but normal free T4It generally resolves without treatment, only treat if TSH > 10
93
What is Goiter?
Enlargement of Glandcan be uniform or diffuse; irregular or multi nodular
94
How is goiter managed?
* Suppression Therapy: thyroid hormone replacement, decreases TSH stimulation* Rapidly enlarging - biopsy* If hypo or hyper treat for the condition
95
Diagnostic Testing: Serum TSH
Primary HypothyroidismPrimary Hyperthyroidism (over-replacement of hypothyroid state)
96
Diagnostic Testing: Serum Free Thyroixine (FT4)
Estimates unbound (free) T4HIGH = HYPER LOW = HYPO
97
Diagnostic Testing: Total Thyroxine
thyroxine is protein bound - drugs and conditions can alter the levelHIGH = HYPERLOW = HYPO
98
Diagnostic Testing: Total and Free T3
useful for diagnosing HYPERthyroidism
99
Diagnostic Testing: Thyroglobulin
papillary or follicular thyroid cancermay indicate: recurrent tumor
100
Diagnostic Testing: Thyroid Antibodies
autoimmune conditionsHYPO: HashimotosHYPER: Graves
101
What thyroid diagnostic test should you order first in an asymptomatic patient?
TSH initiallyif HIGH - T4 to confirm HYPOif LOW - T4 and total T3 HYPER
102
What is thyroid diagnostic test should you order first in a symptomatic patient or patient with risk factors?
Both TSH and free T4
103
Lab Abnormalities in Hypothyroid Conditions: LIPIDS
increased triglycerides and cholesterolnormalizes with treatment
104
Lab Abnormalities in Hypothyroid Conditions: Cellular Enzyme Elevation
CK - suggests myopathyAST and LDH normalizes with treatment
105
Lab Abnormalities in Hypothyroid Conditions: Hyponatremia
associated with SIADHnormalizes with treatment
106
Which patients should be screened for thyroid disorders?
Patients with: Atrial fibrillation, Osteoporosis, Hyperlipidemia, Diabetes Mellitus, Down or Turner's SyndromePatients Taking: Amiodarone or Lithium
107
Radioactive Iodine Uptake Imaging
I131 Used for the evaluation of Nodules"Hot" less likely to be malignant
108
RAIU - Increased Uptake
Grave's Disease
109
RAIU - Decreased Uptake
Silent thyroiditisSubacute thyroiditisPostpartum thyroiditisExogenous hyperthyroidism
110
RAIU - What does hot nodule and cold nodule mean?
Hot - take up iodine - overactive; can overproduce thyroid hormoneCold - under active thyroid
111
Thyroid Ultrasound Uses
following nodulesdetermine character of noduleguidance of fine-needle aspiration
112
drugs that decrease TSH secretion (low serum TSH)
DopamineGlucocorticoids
113
drugs that INCREASE thyroid hormone secretion
IodineAmiodarone
114
drugs that DECREASE thyroid hormone secretion
LithiumIodineAmiodarone
115
drugs that DECREASE T4 absorption
Ferrous Sulfate
116
drugs that INCREASE TBG concentration
Estrogens
117
Management of Hypothyroidism
Lifelong replacement therapyAutoimmune causes - removal or ablation
118
Drug for Thyroid Replacement Therapy and Goal of Treatment
Levothyroxine - stay with same brand (bioequivalency issues)goal: normalize TSH (0.4-2.0 mIU/L)over-replacement if <0.3 risk osteoporosis and atrial fibrillation6-8 weeks to stabilize; once stable check every 6 months to yearly
119
Thyroid Replacement for Healthy Patients
full dose1.6 ug/kg/dayreassess TSH in 6-8 weeks
120
Thyroid Replacement in Elderly Patients or those with Cardiac Disease
start low and go slow
121
Signs and Symptoms of Hyperthyroidism
GoiterSweating of handsWeight lossTirednessPalpitationsRegular Pulse > 90Lid LagDyspnea on ExertionFinger TremorNervousnessExcessive SweatingHot HandsPreference for ColdExopthalmosHyperkinesisDiarrheaScant MensesAtrial Fibrillation
122
What is Apathetic Hyperthyroidism?
elderly patients present with minimal symptomology of hyperthyroidism
123
Signs and Symptoms of Graves Disease
Diffuse Nontoxic GoiterOphthalmopathy: stare, lid lag, exopthalamosDermopathy - pretibial myxedemaThyroid Acropachy - digital clubbing, periosteal reaction
124
Causes of Hyperthyroidism
GravesToxic Multinodular GoiterThyroid NoduleThyroiditisExogenous intakeMedications: Amiodarone; iodineRARE: adenoma, trophoblastic disease, stuma ovarii
125
Complications of Hyperthyroidism
Very distressingAtrial FibrillationCHF, Angina, MI, Sudden DeathOsteoporosis
126
Hyperthyroidism Treatments
Radioiodine ablative therapySub-total thyroidectomyAntithyroid drugsSymptom treatments
127
Radioiodine Ablative Therapy
most common treatment for Gravesgoal of treatment: Hypothyroidism
128
Sub-total Thyroidectomy
goal: leave enough gland to produce endogenous hormonespare: parathyroid glands, recurrent laryngeal nerves
129
Antithyroid Drugs
Propythiomuracil (PTU) and Methimazoledecrease the production of thyroid hormones - important to monitor hormone levelspreferred in pregnant patientsside effects: agranulocytosisseek immediate care for fever or sore throat
130
Symptomatic Treatment of Hyperthyroidism
B-Blockers: tremor and heart rateDiltiazem & Verapamil Clonidine** used until definitive treatment completed
131
What is Thyroid Storm?
Sudden severe exacerbation of thyrotoxicosisoften precipitated by trauma, infection, surgery
132
Symptoms of Thyroid Storm
feversevere tachycardiadelirium
133
Treatment of Thyroid Storm
antithyroid drugs: PTU or methimazolehigh dose glucocorticoidspotassium iodide to suppress further hormone release
134
Thyroid Nodule Risks for Malignancy
prior radiation< 30 years of age; > 60family history
135
Evaluation of Thyroid Nodule
TSH, Free T4 and T3Normal TSH: fine needle aspirationBenign: follow clinicallyMalignant: surgical referral
136
Multinodular Goiter
diffuse processidentified on physical examlow risk of malignancy
137
Subacute Thyroiditis
cause: postvirals&s: anterior neck pain; elevated ESRtx: symptomatic - analgesicstypically recover euthyroid
138
Painless Thyroiditis
autoimmune - leads to long term hypothyroidismno neck discomfortdecreased uptake of radio iodinepostpartum: w/in 1 year of deliverysilent: not associated w/ childbirth
139
FOUR Phases of Thyroiditis
HyperthyroidEuthyroidHypothyroidSome recover to a euthyroid state
140
1. Which of the following is a cell in the body that is capable of differentiating to a plasma cell and secreting antibody: A. B cells B. Mast cells C. Natural Killer cells D. Neutrophils E. Platelets
A. B cells
141
2. The movement of cells from the blood to a site of inflammation due to the release of inflammatory mediators: A. Chemotaxis B. Opsonization C. Phagocytosis D. Pavementing E. Pinocytosis
A. Chemotaxis
142
3. Specificity and memory are the two major characteristics of: A. The adaptive immune system B. The complementary immune system C. The humorous immune system D. The indirect immune system E. The innate immune system
A. The adaptive immune system
143
4. The immunoglobulin that is associated with allergic reactions: A. IgA B. IgD C. IgE D. IgG E. IgM
C. IgE
144
5. The part of an antigen that is recognized by an antibody or T cell receptor: A. Agretype B. Allotype C. Epitope D. Idiotype E. Isotype
C. Epitope
145
6. Which of the following is true of an IgG molecule: A. It actively crosses the placenta B. It has a secretory component C. It has 5 antigen binding sites D. It is a B cell surface immunoglobulin receptor for antigen that is pentameric in structure E. It is the antibody produced on first exposure to antigen
A. It actively crosses the placenta
146
7. The process by which cells non-specifically engulf material and enclose it within a vacuole in the cytoplasm is known as: A. Chemotaxis B. Cytolysis C. Pavementing D. Phagocytosis E. Pragmatism
D. Phagocytosis
147
8. The immunoglobulin that is found predominantly in secretions: A. IgA B. IgD C. IgE D. IgG E. IgM
A. IgA
148
9. Which of the following cells plays a central role in the development of an immune response? A. Macrophages B. Neutrophil C. T-cytotoxic cell D. T-helper cell
D. T-helper cell
149
10. General characteristics of the complement system includes proteins that are: A. Produced by the liver and circulate in the blood B. Produced only in response to antigenic stimulation C. Produced only in the spleen D. Specific for each antigen introduced to the immune system
A. Produced by the liver and circulate in the blood
150
11. Which component is found in both the classical and alternative pathways and is central to complement activation? A. C1q B. C3 C. C5a D. C9
B. C3
151
12. The sum of the attractive and repulsive forces of all antibodies binding to an antigen is: A. Affinity B. Cross –reactivity C. Non-reactivity D Specificity
A. Affinity
152
13. Lysis of cells by complement is finalized by the formation of : A. C1q B. Immune Complexes C. Membrane Attack Complex (MAC) D. Properdin
C. Membrane Attack Complex (MAC)
153
14. Which one of the following statements is TRUE concerning the secondary response to an antigen? A. No memory cells are produced B. The predominant response is IgG. C. The quantity of IgM antibody produced is higher than in the primary esponse D. The specificity of the antibody is different from the primary response.
B. The predominant response is IgG.
154
15. Which of the following can be an antigen presenting cell through MHC Class II: A. Bacterial B. Macrophage C. Neutrophils D. Red blood cells E. T-cells
B. Macrophage
155
16. The cell in the body that has the potential to become a B-cell or T-cell is: A. Bone marrow fibroblasts B. Common lymphoid progenitor C. Common myeloid progenitor D. Fetal liver endothelial cells
B. Common lymphoid progenitor
156
17. T-cells receptors (TCR) and B-cell receptors (surface immunoglobulin) are similar as they: A. Acquire specificity through gene rearrangements B. Are heterodimers C. Have many receptors of only one antigenic specificity D. Have variable and constant regions E. All of the above
E. All of the above
157
18. The binding energy between an antigen and antibody: A. Is non-reversible B. Is reversible C. Is unrelated to the laws of mass action D. None of the above
B. Is reversible
158
19. The class or subclass of an immunoglobulin is determined by the: A. CH region B. CL region C. VH region D. VL region
A. CH region
159
20. Polymorphonuclear granulocytes include: A. B-cells B. Endothelial cells C. Neutrophils D. T-cells
C. Neutrophils
160
21. A T cell receptor recognizes processed antigen; whereas, a B cell receptor recognizes: A. 8-12 amino acids. B. Conformational antigens (approximately 125 amino acids). C. Denatured antigen. D. Linear antigens.
B. Conformational antigens (approximately 125 amino acids).
161
22. Following antigen presentation by a B cell to a T helper cell, cytokines are produced and the B cell: A. Kills the T cell.. B. Rearranges its VDJ and VJ genes. C. Secretes antibody D. Undergoes class switching, becomes a plasma cell and secretes an antibody
D. Undergoes class switching, becomes a plasma cell and secretes an antibody
162
23. Cells determine what peptides are to be presented to the immune system by: A. Chance contact B. Phagocytosis by the T cell receptor C. Presentation through Class I or Class II molecules that have peptides bound to them D. Protein synthesis E. Secreting antibody
C. Presentation through Class I or Class II molecules that have peptides bound to them
163
24. Which one of the following is primarily part of the innate immune response? A. B cells B. Cilia C. T cells D. All of the above E. None of the above
B. Cilia
164
25. The Fab region of the immunoglobulin molecule is important in: A. Activating complement following antibody binding to antigen B. Binding of cells to an antibody that is bound to an antigen C. Binding to an antigen D. Determining the class or subclass of antibody E. Placental transfer
C. Binding to an antigen
165
26. Affinity maturation of the humoral immune response is due to: A. Continued stimulation of B cells by high levels of antigen B. DNA recombination by products of the D region genes C. Isotype switching D. Negative selection of T cells with the lowest helper potential E. Continued stimulation of B cells with low levels of antigen resulting in somatic mutation and the positive selection of B cells with the highest affinity for antigen
E. Continued stimulation of B cells with low levels of antigen resulting in somatic mutation and the positive selection of B cells with the highest affinity for antigen
166
27. Lymphocytes acquire their antigen specificity: A. As they enter the tissues from the circulation B. Before they encounter antigen C. Depending on which antigens are present D. From contact with self antigen E. In the secondary lymphoid organs
B. Before they encounter antigen
167
28. Phagocytosis: A. Can be enhanced by antigen binding to complement or antibody B. Is an antigen-specific process C. Must be preceded by antigen processing D. Rids the body of virus-infected cells E. Only occurs after plasma cells begin secreting antibody
A. Can be enhanced by antigen binding to complement or antibody
168
29. In bacterial infections, T cytotoxic cells do not seem to be very important. This is because: A. They are resistant to the enzymes that T cytotoxic cells release when activated B. Bacteria do not express MHC Class I that is necessary for cytotoxic T cell recognition C. Bacteria do not express MHC Class II that is necessary for cytotoxic T cell recognition D. Bacteria do not express MHC Class I that is necessary for T helper cell recognition
B. Bacteria do not express MHC Class I that is necessary for cytotoxic T cell recognition
169
30. Antigens normally expressed only on embryonic cells but also sometimes found on tumor cells fixed in early development are known as: A. Oncofetal antigens B. HTLV-1 C. Maternal D. Neonatal E. Cryptic
A. Oncofetal antigens
170
31. In the treatment of leukemias, the process of bone marrow purging is performed by: A. Taking out the bone marrow and then just putting it back in B. Taking out the bone marrow, using antibody to the tumor to remove tumor cells and then putting the remaining cells back in C. Taking out the bone marrow, using antibody to the tumor to remove tumor cells and then putting the tumor cells back in D. Taking bone marrow from another cancer patient and putting it into the patient
B. Taking out the bone marrow, using antibody to the tumor to remove tumor cells and then putting the remaining cells back in
171
32. An example of a known oncogenic virus is: A. Herpes zoster B. HIV-2 C. Epstein-Barr virus D. Vesicular stomatitis virus
C. Epstein-Barr virus
172
33. The normal immunological control of tumors is normally through which response: A, Humoral immunity B. Cell mediated immunity C. Innate immune system D. Immunological senescence
B. Cell mediated immunity
173
34. Extracellular bacteria are optimally killed by: A. Macrophages B. Complement C. Antibody D. Macrophages plus complement E. Macrophages plus antibody plus complement
E. Macrophages plus antibody plus complement
174
35. Specific immunity to the intracellular organism M. tuberculosis in mice can be transferred to an uninfected mouse by: A B-cells B. T-cells C. Macrophages D. Neutrophils E. IgG
B. T-cells
175
36. Cytotoxic T-cells: A. Are usually CD4+ B. Recognize native viral antigen C. Kill virally infected cells D. Kill viruses directly
C. Kill virally infected cells
176
37. Protection against worm infestations is particularly associated with an increase in: A. IgD B. IgE C. IgG D. IgA E. IgM
B. IgE
177
T/F: Heavy chains: two for each immunoglobulin molecule and they are identical
True- Light chains are identical too but are either Kappa (80%) or Lambda
178
Immunoglobulin gene rearrangement happens in the presence/absence of antigen?
Absence
179
T/F: Heavy chains have VJ while light chains have VDJ
False
180
_______ Chain rearrangement begins first in the absence of antigen in the primary lymphoid tissues
Heavy
181
___ combines with C which most often codes for IgM constant region or IgD.
VDJ
182
Once VJ try to combine up to 3 times on the light chain, does the cell die?
IgLambda light chain rearrangement occurs only after kappa light chain does not successfully rearrange.
183
T/F: Once rearrangement has occurred successfully, IgM is placed on the cell surface as a receptor?
True- Membrane bound, monomer on the cell surface (sIg), becomes pentamer in circulation, when secreted by plasma cell
184
Germ line theory of diversity: (5 parts)
1) Multiple genes2) Somatic mutation (only with B cells/presence of antigen)3) Somatic recombination4) Gene conversion5) Recombinatorial imprecision
185
Heavy chain re-arrangement occurs following Ig gene rearrangement in the _________ lymphoid tissue and is have antigen/non-antigen dependent.
Secondary, antigen dependent
186
T Cell variability is similar to Ig rearrangements and the mechanism is exactly like B cells except they only have 2 chains. Either alpha (light) and _______ (heavy) chains or ______ (light) and delta (heavy) chains
beta, gamma
187
T cell gene rearrangements occur ___________ for the alpha and beta, or gamma and delta genes
Simutaneously
188
B-cells see ___ amino acids while T-cells see a peptide at ~____ amino acids
125, 10
189
CD3 molecule is always on what type of cell
T cell
190
Anything that starts with "D" is class ____ and everything else (A,B,C) is class ___
2, 1
191
CD4 binds:
MHC class 2
192
All A, B, or C (class 1) have the same basic structure, differ at the __________ site by the peptides they can bind.
Binding- Class 2 looks just like class 1 but has two distinct polypeptide chains
193
Function of Class 1 is to present peptide to the:
T cell receptor- So does Class 2
194
MHC class 1 is found on all ________ cells while MHC class II is found on all _____________ cells
Nucleated (not RBC), antigen presenting cells (Macrophage, dendritic, B cells)
195
Binding of antibodies to antigens is NOT _____ and follows Michaelis-Menton kinetics
STATIC
196
MHC Class II is made in the ________ __________ and the _________ is cleaved into fragments
Endoplasmic reticulum, antigen
197
MHC Class I senses inside/outside cell and presents it to the immune system
Inside- Made in the endoplasmic reticulum as well just like Class II but the difference is INSIDE the cell
198
Cells altered by chemicals, mutations, and viruses that result in immortalization is what and how do they occur?
Tumor: Lose contact inhibition and other growth characteristics thus they do not grow faster, just uncontrolled.
199
Monoclonal comes from ____ cell type
one
200
Oilgoclonal comes from multiple cell types, usually up to __
8
201
Polyclonal is
Multiple cell types usually more than 8
202
What is some evidence immune surveillance exists?
1) Post-mortem. Increased tumors2) Lymphoid infiltrates into tumors are frequently found3) Spontaneous regression of tumors.4) Tumors more in neonatal and elderly period.5) Tumors arrise more in immunosuppressed.
203
Tumor associated antigens are ______ and _________.
Shared and associated- cross reactivity with tumors of common origin
204
If you excise a tumor from a mouse and then inject the mouse with the same tumor, will tumor growth occur? What does this show?
No tumor growth- shows tumor specific antigens
205
Example of normal differentiation antigens: CALLA
Cellular, Acute, Lymphoblastic, Leukemia, Antigen
206
In tumor, you use CD4, CD8, and what else?
Macrophage
207
T cytotoxic cells (CD_+) are capable of killing tumors, but they also need CD_+ T cells for help and direction
8, 4
208
T/F: TH1 cells activates macrophages resulting in type IV hypersensitivity where the host is killing the graft (your tumor)
True
209
T/F: K or NK cells can release enzymes (Perforin and Granzymes) to lyse the cell without antibody
False- need antibody
210
Mechanisms for Tumor to escape Immunosurveilance
1) No tumor specific antigen expressed so nothing for CD8+ or CD4+ to recognize as foreign. 2) Loss of MHC class 1.3) Loss of MHC class 2 to present antigen.4) No appropriate TCR5) Lack of co-stimulatory molecules would actually result in apoptosis6) Blocking of antibody by antigen complexesTHIS IS NEAT :)
211
Active, non-specific, immunotherapy for tumors
Administering immune-modulators
212
Active, specific, immunotherapy for tumors
Therapeutic vaccines of tumor cells, cell extracts, antigens, peptides, proteins, or DNA-pulsed dendritic cells
213
Passive, non-specific, immunotherapy for tumors
Lymphokine activated killer cells are activated in vitro and then placed back in host- no specificity
214
Passive, specific, immunotherapy for tumors
Antibodies alone or coupled to drugs,etc
215
Antibiotic Mechanisms - sulfonamides
competitive antagonism
216
Antibiotic Mechanisms - penicillins
cell wall inhibition
217
Antibiotic Mechanisms - antifungals
cell membrane interference
218
Antibiotic Mechanisms - erythromycin
protein synthesis inhibition
219
Antibiotic Mechanisms - tobramycin
protein synthesis alteration
220
Antibiotic Mechanisms - ciprofloxacin
nucleic acid interference
221
Penicillins
Beta-lactam antibioticsLow toxicityCross-allergenicityG+ coccal infections
222
IM Penicillins
Procaine & Benzathine or combinationcreate low blood levels of drug - used for syphilis
223
Ampicillin/Amoxicillin
Penicillin coverage + H. flu + e.coliused: oral, sinus, skin infectionproblems: diarrhea, allergy, maculopapular rash
224
Amoxicillin/Potassium Clavulanate (Augmentin)
fixed dose amoxicillin combination with B-lactamase inhibitorside effects: GI upset, diarrhea
225
Penicillinase-Resistant Penicillins (2)
OxacillinDicloxacillin
226
1st Generation Cephalosporins
gram-positive cocciCefazolin, Cephalexin, Cefadroxil
227
2nd Generation Cephalosporins
gram-positive cocci, some gram-negative, some anaerobesCefuroxime, Cefoxitin
228
3rd Generation Cephalosporins
gram-positive cocci, > gram-negative spectrum can penetrate CSFCefotaxime, Ceftriaxone, Ceftazidime
229
4th Generation Cephalosporins
gram-positive, increased activity versus enterobacteriacea, pseudomonas
230
Macrolides - Erythromycin uses
penicillin substitute for Mycoplasma, Chlamydia, or campylobacter
231
Macrolides - Azithromycin
more gram-negative coverage than erythromycin
232
Macrolides - Clarithromycin
used is AIDs related infections; H. pylori eradication
233
Ketolide
Telithromycin - macrolide derivativecommunity acquired pneumonias > 18 liver & other toxicities
234
Tetracyclines
Gram-negative rods, rickettsial, chlamydia, lyme disease, acne, penicillin-resistant G+ infectionstetracycline, doxycycline, minocycline
235
Tetracyclines Contraindications & Side Effects
AVOID in pregnancyGI upset, tooth staining, vertigo
236
Clindamycin
aerobic gram-positive cocciproblem: C. difficile overgrowth
237
Vancomycin
used for MRSA, staph epidermidis
238
Fluoroquinolones
DNA gyrase inhibitorsgram negative rods & cocci, psuedomonas, gram positiveCiprofloxacin, Ofloxacin, Levofloxacin, Moxifloxacin
239
Sulfonamide Toxicities
allergic reactionsblood dyscrasias
240
Metronidazole Use
used against anaerobes of GI origin, giardia, bacterial, trichomonal vaginal infections
241
Metronidazole Toxicities
nausea, headache, metallic taste, disulfiram-like reaction with alcohol
242
Antibiotics and Oral Contraceptives
amoxicillin, metronidazole and tetracyclines - interfere with oral contraceptive efficacy
243
T/F: Viruses do not replicate without host machinery?
True
244
T/F: External Antigens, Membrane and capsid of a virus. Antibodies to external antigens are protective 70% of the time- neutralizing antibodies that stop the virus from binding to its receptors.
True
245
Internal antigens of a virus. Mainly the ____________, but antibodies to internal antigens are protective/non-protective?
Nucleocapsid, non-protective
246
Viruses selectively destroy and affect certain tissues because:
Attachment is through the specific receptors
247
Small viruses "slipping" through the membrane by chance and hydrophobicity is called what?
Viropexis penetration
248
Most viruses enter cells in this way:
Receptor mediated endocytosis
249
T/F: Uncoating occurs in the nucleus by enzymes or through phagolysosomal granules
False: occurs in cytoplasm
250
Replication of viruses: DNA viruses replicate in the ________
Nucleus- but both RNA and DNA make protein through mRNA
251
Replication of viruses: RNA viruses replicate in the ________
cytoplasm- but both RNA and DNA make protein through mRNA
252
Immunity to viruses is primarily __ Cell mediated. Explain:
T-cell: Class I restricted cytotoxic cells as all nucleated cells have MHC class I.
253
T/F: In virus infections, you can have Non-neutralizing and neutralizing antibodies?
True- Hopefully you have neutralizing antibodies
254
Interferon (IFN) alpha and beta do what?
Are released by virally infected cells to the surrounding cells. Have the capability of inhibiting viral infection of the uninfected cells.
255
Interferon-gamma causes increased __________
Responsiveness
256
T/F: Bacteria have their own MHC Class I and MHC class II
False
257
Catalase is 1 way bacteria escape phagocytosis. What does catalase break down?
Hydrogen peroxide
258
If you have a bacterial abscess and cut it open, what 4 things would you most likely see from bacterial immunity?
Antibody, macrophages, neutrophils, complement. Mediated by CD4 T helper cells.
259
Immunity to fungi: Primarily cell mediated through:
MHC Class I and Class II- probably through some antigen presentation through dendritic cells
260
Important cells in parasite immunity:
T cells, macrophages (directly killing it or effector cells release cytokines), B cells (produce IgE- wash out parasite). Look at end of Immunity to fungi lecture for a chart if you want more detail.
261
Fever CriteriaRectal:Oral:Axillary:
Rectal: 100.4 F or 38 COral: add 1/2 degree, starts at 99.9 FAxillary: add 1 degree, starts at 99.4 FAural - accurate if perfect seal achieved
262
Fever Without a Source
children with a fever lasting for one week or less without adequate explanation after a careful history and thorough physical examination
263
Fever of Unknown Origin
fever > 101 F of at least 8 days durationno diagnosis apparent after initial outpatient or hospital evaluation
264
All babies 3 months or younger with a fever of 100.4 or higher MUST
BE SEEN THAT SAME DAY!
265
Fever in Infants < 3 months: Bacterial S&S
bacterial infectionss&s: low grade fever, poor feeding, irritability, sleepiness/sleeplessness
266
Fever in Infants < 3 months: History
Associated Symptoms: respiratory, GI, ENTBehavioral Symptoms: poor feeding, irritability, poor sleeping, abnormal cryExposure to Sick Contacts: siblings, babysitter, day carePrevious IllnessBirth History
267
Fever in Infants < 3 months: Physical Exam
GestaltAbnormal Vital SignsToxic AppearanceSigns of Localized Infection
268
Toxic Appearance
irritabilityinconsolabilitypoor perfusionpoor tonedecreased activitylethargy
269
Common Pathogens < 3 months - Bacteremia
S. pneumoniaeHibgroup B strepN. meningitissalmonellaListeria monocytogenes
270
Common Pathogens < 3 months - UTI
E. coli
271
Common Pathogens < 3 months - Pneumonia
S. aureusS. pneumoniaegroup B strep
272
Common Pathogens < 3 months - Meningitis
S. pneumoniaeHibgroup B strepmeningococcusherpes simplexenterovirus
273
Sepsis Evaluation
CBC w/ differentialSerum GlucoseLumbar PunctureBlood CultureUrine CultureInflammation Indicators: ESR, CRP, ProcalcitioninConsider: stool culture, CXR
274
When to admit fever in infant < 3 months for empiric antibiotics? (3)
Toxic Looking< 1 month of agePoor social situation
275
Outpatient Observation Fever < 3 months
Option 1: blood culture, urine culture, lumbar puncture - Ceftriaxone - re-evaluate in 24 hoursOption 2: urine culture, careful observation
276
Fever in Children < 3 years
most illness in this age group are self-limited viral infectionsincreased risk of occult bacteremia
277
Common Pathogens for Fever in Children < 3 years
S. pneumoniaeHibN. meningitisnon-typhoidal SalmonellaUTI and pneumonia are possible causes of occult infection
278
Fever in Children < 3 years - History
Functional Status: oral intake, activity level, irritabilityCough, Vomiting, Dysuria, Frequency, Potty AccidentsImmunization Status!!!!
279
Physical Exam Children 3-36 Months - Findings warranting extra attention
Toxic AppearingCyanosisHypo/HypervenilationAbnormal Vital Signs - SpO2 < 95%TachycardiaTachypneaLesions in OropharynxAbdominal TendernessPain with bone palpation or passive ROMPetechiae, cellulitis, viral exanthem
280
Gestalts in feverish children < 3 years
AlertnessPlayfulnessIrritabilityConsolability
281
Risk Factors for Occult Bacteremia
Temp > 102.2 FWBC > 15,000/mm3Elevated neutrophils or bandsElevated ESR, CRP or PCT
282
What type of fever has:high spike and rapid resolution
Intermittent FeverTB, lymphoma, JIA/JRA
283
What type of fever has:fluctuant peaks, but doesn't return to normal
Remittent Feverviral, endocarditis, sarcoid, lymphoma, atrial myxoma
284
What type of fever has:fever persists with little fluctuation (unless meds given)
Sustained Fevertyphoid fever, typhus, brucellosis
285
What type of fever has:fevers that relapse after 1 or more days with no fever
Relapsing FeverMalaria, rat-bite fever, Borrelia infection, lymphoma
286
What type of fever has:episodes of fever more than 6 months duration
Recurrent Feverother causes: metabolic defects, CNS abnormalities, immunodeficiency
287
Fever of Unknown Origin
weight lossdrug/medicationsimmunizationsimmunosuppressive therapyPicaexposure to soil borne or water borne organismshistory of blood transfusionstravelexposure to animalsticks of mosquitosrecent surgery or dental worktattoos, body piercingsexual activity
288
Fever of Unknown Origin - Skin Examination
presence of sweatingpetechiaerashsparse hair
289
Fever of Unknown Origin - Eye Examination
ConjunctivitisRetinopathyAbsence of pupillary responseAbsent tears or corneal reflexesAbnormal fundoscopic exam
290
Fever of Unknown Origin - Oropharynx Examination
Hyperemia of posterior pharynxDental abscessAbnormal DentitionSmooth tongueGinigival Hypertrophy
291
Fever of Unknown Origin - Lymph Node Examination
Enlarged and/ore multiple lymph nodes
292
Fever of Unknown Origin - Chest Examination
CracklesNew onset murmur
293
Fever of Unknown Origin - Abdomen Examination
OrganomegalyTenderness with liver palpation
294
Fever of Unknown Origin - Musculoskeletal
Tenderness to bones or musclesHyperactive DTRs
295
Fever of Unknown Origin - GU
STD testingCareful exam for any masses or abscessesStool should be examined for occult blood
296
An antibody to an Antigen is known as an immune what?
Complex
297
With the classical complement pathway, you need what to activate it?
Antibody binds to antigen
298
What activates C3 in the alternative pathway?
H2O
299
C3 convertase in classical pathway? C3 convertase in alternative pathway?
Classical= C4b2aAlt=C3bBb
300
Ultimately, the complement pathway ends by doing what to the cell?
Lysis by MAC attack
301
T/F: C5 activates adhesion molecules on macrophages?
True
302
What cell controls other cells (macrophage, granulocyte, NK cell,etc. or in Thiele's terms, is the "mother" of all cells?
T-Helper cells
303
T-Cytotoxic cells are important in recognition and killing by what mechanism?
Granules: Lyse (perforin) and enzymes
304
T helper cells: CD4 or CD8? Sees how many amino acids?
CD4+, CD4 binds MHC class II, looks for peptide in groove and sees 8-14 amino acids
305
T cytotoxic cell: CD4 or CD8 and sees how many amino acids?
CD8+, CD8 binds MHC class I and looks for peptide in groove. Sees 8-14 amino acids. On all nucleated cells!!
306
What are B cells?
Surface Immunoglobulin (sIg)= receptor for an epitope on an antigen. Also an antigen presenting cell. Sees 125 amino acids
307
Linked recognition means what?
Process by which a TCR and a sIg recognize different epitopes on the same antigen, thus linking their response
308
If you perform a transplant, you want to knock out what?
CD4
309
T/F: Overweight at age 4=20% chance in adulthood.
True
310
BMI Standards for Overweight, Obese (Class I and II), and Morbidly obese
BMI>25= overweightBMI>30= obese Class 1:30-34.9, Class 2: 35-39.9BMI>40 Morbidly obese*Different for CHILDREN!BMI=Weight (kg)/Height (m) ^2
311
Children BMI percentile ranges
-BMI between 85-95th%ile = At risk for obesity-BMI>95th%ile = Obese
312
Obesity patterns: Android
Truncal Obesity= Increased incidence of morbidity and mortality
313
Obesity Patterns: Gynecoid
Hip/Gluteal obesity
314
Other measures than BMI for Obesity
-Waist-to-hip ratio: >1.0 males and >0.85 females-Abdominal Circumference: >102cm males and >88cm females
315
What is most basic cause of Obesity?
Calories in vs. calories out= energy intake exceeds energy use.
316
Some multifactorial causes of obesity:
1) Genetics (Leptin, etc.) with interaction of environment.2) Environmental (Sleep, smoking cessation, social, dietary factors, etc.)3) Endocrine4) Medications5) Psychological
317
Prenatal Influences on obesity:
-MOM: Pre-pregnancy BMI and gestational weight gain.-BABY: LBW, short stature, small head circumference= increased risk for abdominal fatness.-Breastfeeding vs. formula feeding -Genetic and Environmental factors
318
Neuroendocrine Causes of Obesity
Cushings Syndrome, Hypothyroidism, Polycystic Ovary Syndrome, Growth hormone deficiency, "Hypothalamic obesity"-Signs for women may be Hirsutism
319
A congenital etiology of obesity
Prader-Willi Syndrome
320
List some Comorbidities of obesity
Metabolic syndrome, Insulin resistance, DM II, HTN, CV disease, Dyslipidemia, Respiratory problems, Sleep apnea, hernias, reflux, stress incontinence, hemorrhoids, skin problems, psychologic.
321
Associated comorbidities of Obesity
-Venous problems, Increased risk of cancer, GI problems
322
Acanthosis nigricans is a sig of elevated _________ levels
Insulin. Early insulin resistance and DM II
323
1st line Treatment for an adult with Obesity
- Decrease caloric intake by 500-1000 cal.day. Need 1000-1200/day, 1200-1500 (men)-Increase physical activity (30-60 min most days per week (5x)-Support group-Nutritional consult-Lifestyle modification (goal is 2#/week, 8-10% of baseline weight)
324
2nd line Treatment for an adult with Obesity (Classes of Medications)
-As an adjunct to diet and exercise. -BMI >30 or BMI 27-29.9 and comorbid condition.-MEDICATION classes: Catecholaminergic medications, Drugs that alter digestion, SSRIs, Combinations of "older medications"
325
Sympathomimetic (Catecholaminergic) medictions for obesity
1) Phentermine (Fastin)- stimulant2) Sibutramine (Meridia)
326
Drugs that alter digestion for Obesity
1) Orlistat- Decrease fat absorption (OTC is Alli)
327
Serotonin Agonists for Obesity
-Loracaserin-Fluoxetine (Prozac) and Bupropion (Wellbutrin)
328
Surgical treatment for Obesity and requirements.
- Bariatric Surgery: Only morbidly obese (BMI>40) who have tried weight loss methods and failed or patients with BMI>35 and have comorbid condition-Gastric bypass-Gastric banding
329
What should be present with all treatment options in obese patients?
Behavioral therapy- Alter eating and physical activity habits
330
Beta-lactams are effective against Gram +/ Gram Negative?
Gram Positive
331
Beta Lactams bind
penicillin binding proteins blocking cross linking causing cell death
332
MRSA has altered Penicillin Binding protein and decreased affinity for all B-lactams. This was likely acquired from:
Coag-negative Staph
333
Vancomycin binds to
Cell wall precursors
334
T/F: Vancomycin Resistant Enterococci (VRE) use alternative precursors for cell wall, vanA and vanB are most common genes, and acquired from environment and other strep species?
True
335
T/F: VRSA was first seen in 2002 with few reports and all the organisms contained the vanB gene?
False: contained vanA
336
Which of the following does not have activity against MRSA?A) BactrimB)ClindamycinC) ErtapenemD) LinezolidE) Tigecycline
C) Ertapenem- B-lactam drug
337
Treatment for S. Aureus skin and soft tissue infections:A) For a boilB) MSSAC) MRSA
A) Surgical drainage- usually adequateB) Oxacillin/NafcillinC) Vanco, Linezolid, Daptomycin, Tigecycline
338
What antibiotic causes C. difficile?
Clindamycin
339
T/F: Linezolid is superior to vancomycin for treating MRSA pneumonia
False: Equivalent
340
Therapy for MRSA pneumonia
Start with Vancomycin, then linezolid. Do not use Daptomycin (inactivated by surfactant)
341
Therapy for MRSA Bacteremia
Start with Vancomycin, then Daptomycin
342
What are 3 mechanisms that decrease permeability in gram negative organisms?
1) Decreased porin expression2) Active efflux pumps3) Multi-drug efflux pumps
343
Definition of multidrug-resistant
Resist at least one agent in 3 or more classes
344
What class of drugs was created to overcome Beta-lactamases?
3rd generation cephalosporins
345
4 risk factors for extended spectrum Beta lactamases (ESBL) are:
Location, Antibiotic use, Severity of illness, Devices
346
Clinical presentations of ESBL infections:
UTI, Wound infections, pneumonia, intra-abdominal infections
347
Which of the following is the drug of choice for severe ESBL producing organism infections?A) FQB) TMP/SMXC) CefepimeD) Piperacillin/tazobactamE) Carbapenems
E) Carbapenems
348
T/F: You can use cephalosporins for ESBL treatment
False. DO NOT USE!
349
Carbapenamases hydrolyze all:
Beta-lactams
350
What can make Klebsiella pneumoniae and E.coli highly resistant to almost every drug?
NDM-1: New Delhi Metallo-beta-lactmase 1
351
Treatment for Carbapenemase Producers
No beta lactams. Colistin (nephrotoxic, neurotoxic)? Tigecycline (increased mortality)?
352
Mutation in DNA gyrase and/or topoisomerase IV are alteration in enzymes leading to what type of resistance?
Quinolone resistance in gram-negative pathogens
353
Endocrine vs. Exocrine
ENDO is hormones secreted internally and EXO is secreted externally or into the lumen
354
Palpable endocrine glands
Thyroid, Gonads
355
Primary evaluation of the endocrine system is:
Measuring hormone concentrations
356
Functions of hormones (3)
Growth, Maintenance of homeostasis, reproduction
357
Presentation of Cushing Syndrome
Central fat redistribution, striae, proximal muscle weakness, hirsutism, elevated BP, increased BMI, "buffalo Hump"
358
What is it? Lethargy, weakness, psychomotor retardation, cold intolerance, constipation, hair loss, dry skin, and weight gain
Presentation of hypothyroidism
359
Appropriate screening for hypothyroidism
TSH, confirm free T4
360
What is it? 24 y.o. M with extreme feeling of weakness, 20# weight loss, change in skin color (hyperpigmentation), lightheadedness and dizziness, BP=90/70, Na+ decreased, K+ increased, serum urea increased, calcium increased
Addison Disease
361
What is it? 22 y.o. women with breast secretions, amenorrhea, and decreased libido, BP=140/80, no other symptoms or abnormalities
Hyperprolactinemia most likely from a benign (posterior) pituitary tumor
362
T/F: You see a patient 55y.o. with for the first time and no other previous medical records who has a FPG of 235 mg/dL. You can diagnose this patient with Diabetes Type II
False: Must be confirmed on another day by any one of the criteria
363
Diagnostic criteria for DM type II
-Random glucose >200mg/dL-Fasting serum glucose > 126mg/dL-Serum glucose level >200 mg/dL obtained 2 hours after a 75-g glucose challenge (should be obtained after 72 hours of eating 300 g of carbohydrate per day)
364
Tests NOT used in initial diagnosis of DM II
Insulin levels, C-peptide levels, screening for autoantibodies
365
Prediabetes criteria and what does this mean
Fasting serum glucose of 100-125 mg/dL- Indicates increased risk of progressing to diabetes, may be associated with onset of insulin resistance, commonly a part of Metabolic syndrome
366
Metabolic syndrome criteria
Insulin resistanceHypertensionDyslipidemia (Trigs >150 or HDL-C<40)Abdominal obesity
367
Fasting glucose levels that indicate significant beta cell failure
200 mg/dL
368
In treatment of DM II you should always start with what?
Therapeutic Lifestyle Modification
369
Patients with FPG < 250 mg/dL should be treated how
- Medical nutritional therapy, exercise program. If not controlled in 3 months, move to next step
370
Patients with FLG > 250 but <400 mg/dL who do not have signs of dehydration, acidosis or marked ketosis
In addition to medical nutritional therapy, begin monotherapy with an oral antidiabetic agent (metformin)
371
T/F: Patients with marked elevated FPG and ketonuria or ketonemia or symptomatic patients may require require insulin therapy initially to overcome glucose toxicity?
True
372
What is considered best first line agent for DM II?
Metformin
373
Do not use or use metformin cautiously in what patients?
Do not use in Pts prone to lactic acidosis, if serum creatine is elevated, use cautiously in renal and hepatic disease
374
If blood glucose is severely elevated, you should use what therapy
Sulfonylureas (Glyburide, Glipizide)- May be 1st choice in lean persons who have more pancreatic dysfunction than insulin resistance
375
a-glucosidase inhibitors are most effective in persons with
Mild fasting hyperglycemia, predominantly postprandial hyperglycemia
376
An agent used in adjunct to oral agents (Metformin and/or sulfonylureas) that is given as SQ injection and is an Incretin mimetic
Exenatide/ Liraglutide
377
Shin spots are:
Pigmented atrophic macular areas on the skin over the tibia frequently seen in diabetic patients
378
Necrobiosis Lipoidica is:
Cutaneous sign associated with DM, an irregular erythematous patch, occurs anywhere on the legs, 2-10cm
379
Inability to perceive monofilament indicates
Advanced neuropathy
380
Medical management of Diabetic neuropathy
-Specific: Duloxetine (Cymbalta)-Gabapentin, Amitriptyline, other neurostabilizers (Carbamazepine), Analgesics (NSAID, Acetaminophen)
381
Onset of nonproliferative retinopathy is indicated by:
Microaneurysms (early findings). Proliferative retinopathy with neovascularization/hemorrhages
382
Diabetic patients with BP over what needs medication
135/85- ADA recommends lowering BP to 130/80 mmHg or less
383
Diabetics with LDL greater than what need lipid lowering therapy
130 mg/dL- Target LDL is 100, maybe even as low as 70
384
Emergency complications of DM (3)
1) Diabetic ketoacidosis2) Nonkinetic hyperosmolality syndrome3) Hypoglycemia (insulin reaction)
385
Etiology of Dm type 1
-Autoimmune process. Most common is Hashimotos Thyroiditis. Celiac Disease is another associated autoimmune disease. Antibodies destroy insulin producing beta cells of pancreas (islet cells). -Environmental: Cows milk before 2, Viral infections? Inconclusive
386
What is the most common pediatric endocrine disorder?
DM1
387
Some symptoms of DM1
Multi-organ system involvement: Tiredness, confusion, retinopathy, glaucoma, deep rapid breathing, thirst, vomiting, heart disease, muscle weakness, excessive urine production, weight loss, nerve damage, poor circulation, skin prone to infection
388
Presentation of DKA
Polyuria, Polydipsia, nausea, vomiting, abdominal pain, tachypnea, fruity odor to breath
389
A 12 year old female with DKA. What potential side effect do you want to avoid with treatment?
Cerebral edema- get an endocrinologist involved
390
How to treat dehydration in a DM1 patient
glucose free isotonic solution
391
How to correct hyperglycemia
Fast acting insulin (decrease at 100mg/dl/hr)
392
How to treat acidosis
Should be corrected with insulin- bicarb only in severe cases
393
How to treat electrolyte imbalance
Potassium needs to be replaced
394
Therapy for DM1: Usual starting dose of insulin
0.5U/kg: 50% given to provide basal coverage, 50% divided doses for rapid acting insulins
395
Long acting insulins
Used for basal coverage: Insulin glargine (Lantus), Insulin detimir (Levemir). Not used in pump
396
Rapid acting synthetic insulin
Insulin lispro (Humalog), Insulin aspart (Novolog), Insulin glulisine (Apidra). Completely gone within 3 hours, used in pumps
397
Hypoglycemia results from an ______ of insulin in relation to the serum glucose concentration. Symptoms include: and the Treatment is:
Excess.Symptoms: Headache, visual changes, confusion, irritability, seizures, tremors, tachycardia, diaphoresis, anxiety.Treatment: Fast acting glucose- glucose tabs, soda, juice
398
Goal for A1c in a DM1 patient
<7.0%
399
DM1 phenomena: Honeymoon period
Some beta cells still function. See a decrease need of treatment. Occurs in first few weeks of treatment. Can last a few weeks to couple years.
400
Somogyi Phenomenon
Early morning hyperglycemia that is actually caused by hypoglycemia at night.
401
Dawn Phenomenon
Early morning hyperglycemia caused by early dosing of evening insulin and secretion of GH in early morning hours
402
DM1 preventative care
-Hgb A1c every 6 mos.-Ophthalmologic exams every year-Urine checked for microalbuminuria every year-Annual cholesterol measurements-Monitoring of blood pressures-Thyroid blood tests every year-Daily home foot exams and at every visit
403
Decrease in C-peptide plus diabetic symptoms is what type of diabetes?
Type 1
404
Normal C-peptide plus symptoms is what type of diabetes
Type 2
405
Diabetic ketoacidosis occurs in undiagnosed or uncontrolled DM1. DKA is present when Arterial pH is_____ and Bicarb level is ________ and the ketones are _________ in serum or urine
Less than 7.25, <15mEq/L, Elevated
406
Syndrome X and Insulin resistance is also known as
Metabolic Syndrome
407
Risk Factors for Metabolic syndrome
Abdominal obesity (M=40, F=35)Elevated BP (130/85)Elevated Triglycerides ( >150)Elevated FBG (>110)Low HDL (Males<50)
408
T/F: Patients with Metabolic syndrome are typically symptomatic before complications occur
False: Typically asymptomatic until they develop 1 or more complications (Ex: BP>130/85, Abdominal obesity)
409
Diagnostic criteria for Metabolic Syndrome
If 3 risk factors are presentAbdominal obesity (M=40in, F=35in)Elevated BP (130/85)Elevated Triglycerides ( >150)Elevated FBG (>110)Low HDL
410
Supporting lab tests for Metabolic Syndrome
Abnormal liver fxnIncreased CRPIncreased Uric acidMicroalbuminIncreased serum testosterone in women May be appropriate to order: Cardiac stress test, carotid US, Coronary Calcium scoring
411
What are therapeutic life changes (TLC) for Met. Syndrome
Weight loss (Mediterranean Diet)Dietary modificationsIncrease aerobic exercise (30 min daily)
412
Along with weight loss, balanced diet, and exercise, what other therapy should you give a patient with Metabolic Syndrome to prevent DMII?
Metformin
413
MetS: Treatment for cardiac risk factors:
-HMG-CoA reductase inhibitors (Statin)-Gemfibrozil-Diet, exercise, weight loss
414
Treatment for Obesity
Bariatric surgeryOrlistat, Sibutramine
415
What has been associated with a 2 to 3 fold increase in risk for CHD/Stroke along with 2-fold increase risk of CV mortality?
Metabolic Syndrome
416
Leading cause of death in the US?
Cardiovascular Disease (CVD)- associated with high cholesterol and lipids with decreased HDL
417
NCEP ATP III risk determinants for CHD: HDL
Optimal: >60Borderline High 40-59High Risk >40
418
NCEP ATP III risk Categories
-Low risk: 0-1 risk factor-Moderate risk: >2 risks; 10yr risk -Moderately high risk: 2 risks; 10yr risk 10-20%-High: CHD or CHD risk equivalents; 10-yr risk >20%
419
T/F: A very high risk patient for CHD has LDL >100. Should you consider drug therapy?
Yes
420
You have a moderate high risk patient with LDL <130, should you start therapy?
It is optional. >130 start therapy.
421
When do you start therapy for moderate risk patient for CHD
LDL >160
422
Low risk patient for CHD. When should you start therapy?
LDL >190
423
High risk patients with high TG or low HDL levels what should you consider?
Fibrate or nicotinic acid
424
Pattern of Dyslipidemia in DMII patients
High trigs, low HDL, Qualitative changes in LDL
425
Patient with diabetes should get their LDL below what
<100 without CVD
426
Fibrate can do what to your trigs and HDl levels
Decrease Trigs, increase HDL
427
Niacin (nicotinic acid) can do what to trigs and HDL levels?
Decrease trigs, increase HDL- can cause flushing
428
Ezetimibe (Zetia) can do what?
Further decrease LDL levels by selectively inhibiting intestinal absorption of cholesterol
429
Bile acid sequestrants may do what
Decrease LDL
430
What is lifestyle changes dont decrease lipid levels? What should you prescribe next
Statin- follow up in 6wk to check labs. No improvement, increase dose
