Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Adult/Ped Medicine Cumulative Final > Exam 5 > Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Subcutaneous (SQ)Route of Vaccine Administration

A

Usually “pinch” the skin and inject into fatty tissue under the skin. MMR & Varicella

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pneumococcal Conjugate Vaccine (PCV):Contraindications/Precuations

A
  • known hypersensitivity

* moderate to severe illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pneumococcal Conjugate Vaccine (PCV):Side Effects

A
  • Local erythema
  • Induration
  • Tenderness
  • Fussiness
  • Low grade to moderate fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

MMR Vaccine Measles, Mumps, Rubella Contraindications & Precuations

A

Contraindications:

  • Anaphylaxis
  • Pregnancy
  • Immunodeficiency Precautions:
  • Recent immune globulin administration
  • History of thrombocytopenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

MMR Vaccine Measles, Mumps, Rubella Side Effects:

A
  • Local tenderness/swelling
  • Fever 7-10 days after
  • Morbiliform rash
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Active Immunity

A

Vaccination with live, live attenuated, or inactivated organisms, their components or their products to stimulate protective immunologic response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Meningococcal Vaccine - MPSV 4

A

Children age 2-10 in susceptible children

  • Complement deficiency
  • Anatomic or functional asplenia
  • Other high-risk groups
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Varicella Vaccine: Side Effects

A
  • Local tenderness

* varicelliform rash within 1 month

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Influenza Vaccine Administration

A
  • First dose: 6 months
  • Dose yearly – vaccine typically updated.
  • After age 2, option of live-attenuated (nasal spray).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Influenza Vaccine Precautions

A
  • Avoid in asthma, wheezing past 12 months, underlying medical conditions.
  • Avoid if egg allergy.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Injectable Polio Vaccine (IPV) Side Effects

A
  • VAPP with OPV
  • Hypersensitivity
  • Guillan-Barre??
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Immunogenic Components of Bacteria Vaccines

A

Pertussis, Haemophilus influenzae type B, Streptococcus pneumoniae Toxoids – Diphtheria, Tetanus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Inactivated/Killed Vaccines

A

Polio, Hepatitis A, Influenza

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

HPV Vaccine

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Passive Immunity

A

Trans-placental transfer of maternal antibodies Administration of antibodies, either as:Immunoglobulin, ORMonoclonal antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Heptatis A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Common Vaccine Side Effects

A
  • Localized tenderness
  • Localized erythema
  • Fever
  • Fussiness
  • Allergic reaction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Other Ingredients in Vaccine

A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Hepatitis B Vaccine Who gets it:

A

Universal hep B immunizations in infancy as well as children and adolescents who missed immunization during infancy or those who are at increased risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Hepatitis B Vaccine Administration

A

Given IM (intramuscularly) 1st dose – at birth (within 12 hours) 2nd dose – 1-2 months 3rd dose – 6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Hepatitis B Vaccine Contraindications and Side Effects

A

Contrindications: none SE:Localized tenderness, rare hypersensitivity, reaction to yeast or vaccine preservatives

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Live attenuated vaccinations

A

Measles, mumps, rubella, varicella Live Attenuated is the actual viruses – weakened or altered so that the child doesn’t get sick. These vaccines STING!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is responsible for inflammation?

A

Inflamasome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Humoral adaptive or acquired immune system includes:

A

B Cells, plasma cells, antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Cellular adaptive or acquired immune system includes:

A

T cells, macrophages, neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

80-90% of all immune responses occur through which branch of the immune system?

A

Innate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Histiocytes are macrophages in the:

A

Tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

True/False: Mononuclear phagocytes have a role in both adaptive and innate immunity?

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the predominant cell making up the white cell count?

A

Neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

True/False: The host produces PAMPs.

A

False: host does not produce PAMPS so the innate system does not have to discriminate self from non-self.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are PAMPs recognized by?

A

PRRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

PRRs on phagocytes results in: (4)

A

1) Phagocytosis2) Opsonization through acute phase proteins3) Elevated anti-microbial activity4) Up-regulation of A) adhesion molecules, B) Co-stimulatory molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is opsonization?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Eosinophils are important in:

A

Parasitic infections, allergies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Mast cells are important in:

A

allergies and anaphylaxis: Contain pre-formed histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Basophils during inflammation release potent _________ that exacerbate the response. The granules stain ______

A

Mediators, blue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

_____________ have high nuclear to cytoplasmic ratios and include T-cells, B-cells, and NK cells

A

Lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What cells react with tumor cells and virally infected cells and kill them through apoptosis and enzymes?

A

Natural Killer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

T/F: Acute phase proteins help in opsonization because cells have receptors for these acute phase proteins on their cell surface?

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is the major coordinator of inflammation and made up of over 20 different proteins?

A

Complement (Part of Innate Immune system)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

A group of proteins that have an effect on other cells:

A

Interferons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

T/F: Alpha or beta interferons infect adjacent cells?

A

False: They stop infection of adjacent cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What interferon works through the adaptive immune response to activate T cells and macrophages?

A

Gamma interferon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

In acute inflammation you tend to have higher numbers of what cells?

A

Neutrophils and activated T helper cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

In chronic inflammation you tend to have higher numbers of what cells?

A

Macrophages, t cytotoxic, and B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

A glycoprotein secreted by a plasma cell that is specific for an epitope on an antigen is what?

A

An antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Fab is the fraction of _________ ___________ while Fc is fraction of _______________.

A

antigen binding, crystallization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

T/F: The TCR is secreted

A

False- never secreted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

T/F: T and B memory cells are produced following antigen stimulation?

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

The biologically relevant portion of an antibody is what?

A

Fc (Fraction of crystallization)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Antibodies functionality is conferred by: (4)

A

1) Fc receptors on cells2)Complement activation3) Complement receptors4) Placental transfer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

T/F: IgM crosses the placenta

A

False

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

T/F: IgM is a pentamer

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

T/F: IgM is first immunoglobulin secreted upon antigen stimulation

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

T/F: IgE has an extra piece on the Fc portion that makes it bind only to mast cells

A

True- In the absence of antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

IgA is found in __________

A

Secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Ig__ functions as a marker of maturation

A

IgD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

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)

A

Isotype, Allotype, Idiotype

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

T/F: If IgM is present in the baby, the baby is responding?

A

True: If IgG is present, do not know if it is from mom or baby

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What thyroid hormone is the major product of the thyroid gland?

A

T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What thyroid hormone is active at the cellular level?

A

T3biologically more active; shorter half life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Primary hypothyroidism affects what level?

A

Gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Secondary hypothyroidism affects what level?

A

Pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Tertiary hypothryoidism affects what level?

A

Hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Describe the hypothalamic-pituitary-thyroid axis:

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Describe the spectrum of presentation of hypothyroidism (3).

A
  1. Subclinical hypothyroidism (elevated TSH, normal T4)2. Symptomatic disease3. Severe myxedema coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Etiologies of Primary Hypothyroidism (9)

A
  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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Etiologies of Secondary Hypothyroidism (3)

A

caused by insults to the pituitary gland1. Neoplasm2. Infiltrative3. Hemorrhage into the gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Etiologies of Tertiary Hypothyroidism (4)

A
  1. Neoplasm2. Infiltrative Disease3. Anorexia Nervosa4. Cerebrovascular or surgical insult
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What causes systemic symptoms of hypothyroidism?

A

lack of T3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Frequent Signs and Symptoms of Hypothyroidism(all of the signs and symptoms are listed)

A

WeaknessEdema of faceLethargyCourse SkinSlow MovementsEdema of EyelidsSensation of ColdHoarsenessPeripheral EdemaDry SkinDecreased SweatingPallor of LipsSlow speechCold SkinConstipationThick TongueParesthesiasGain in weightMuscle WeaknessSlow cerebration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Typical Symptoms of Hypothyroidism (6)

A

fatigueweaknesscold intoleranceconstipationweight gaindeepening of voice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Cutaneous Symptoms of Hypothyroidism (4)

A

dry, scaly, yellow skinnon-pitting waxy edema of the facemyxedemathinning of eyebrows

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Cardiac Symptoms (3)

A

bradycardiaenlarged heartlow voltage electrocardiogram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Hypothyroidism Symptoms in the Neck (5)

A

PainSwellingTendernessNodulesCystsor could be asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Neurological Symptoms of Hypothyroidism (3)

A

ParesthesiaAtaxiaProlongation of DTR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Describe the hormone levels in HYPOthyroidism - TSH and T4

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What is Hashimoto’s Disease? What markers will be present?

A

Autoimmune thyroiditisPositive test for antibodies - Anti-Tg and Anti-TPO10 x more common in women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is subclinical hypothyroidism? How is it treated?

A

Elevated TSH with normal free T4TSH > 10: treatTSH 5-10: monitor or possible trial of hormone replacement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What is Acquired Transient Central Hypothyroidism also known as Euthyroid Sick Syndrome?

A

Extremely ill patients with non thyroidal illnessEuthyroid with elevated TSH but normal free T4It generally resolves without treatment, only treat if TSH > 10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is Goiter?

A

Enlargement of Glandcan be uniform or diffuse; irregular or multi nodular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

How is goiter managed?

A
  • Suppression Therapy: thyroid hormone replacement, decreases TSH stimulation* Rapidly enlarging - biopsy* If hypo or hyper treat for the condition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Diagnostic Testing: Serum TSH

A

Primary HypothyroidismPrimary Hyperthyroidism (over-replacement of hypothyroid state)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Diagnostic Testing: Serum Free Thyroixine (FT4)

A

Estimates unbound (free) T4HIGH = HYPER LOW = HYPO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Diagnostic Testing: Total Thyroxine

A

thyroxine is protein bound - drugs and conditions can alter the levelHIGH = HYPERLOW = HYPO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Diagnostic Testing: Total and Free T3

A

useful for diagnosing HYPERthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Diagnostic Testing: Thyroglobulin

A

papillary or follicular thyroid cancermay indicate: recurrent tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Diagnostic Testing: Thyroid Antibodies

A

autoimmune conditionsHYPO: HashimotosHYPER: Graves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What thyroid diagnostic test should you order first in an asymptomatic patient?

A

TSH initiallyif HIGH - T4 to confirm HYPOif LOW - T4 and total T3 HYPER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What is thyroid diagnostic test should you order first in a symptomatic patient or patient with risk factors?

A

Both TSH and free T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Lab Abnormalities in Hypothyroid Conditions: LIPIDS

A

increased triglycerides and cholesterolnormalizes with treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Lab Abnormalities in Hypothyroid Conditions: Cellular Enzyme Elevation

A

CK - suggests myopathyAST and LDH normalizes with treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Lab Abnormalities in Hypothyroid Conditions: Hyponatremia

A

associated with SIADHnormalizes with treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Which patients should be screened for thyroid disorders?

A

Patients with: Atrial fibrillation, Osteoporosis, Hyperlipidemia, Diabetes Mellitus, Down or Turner’s SyndromePatients Taking: Amiodarone or Lithium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Radioactive Iodine Uptake Imaging

A

I131 Used for the evaluation of Nodules”Hot” less likely to be malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

RAIU - Increased Uptake

A

Grave’s Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

RAIU - Decreased Uptake

A

Silent thyroiditisSubacute thyroiditisPostpartum thyroiditisExogenous hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

RAIU - What does hot nodule and cold nodule mean?

A

Hot - take up iodine - overactive; can overproduce thyroid hormoneCold - under active thyroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Thyroid Ultrasound Uses

A

following nodulesdetermine character of noduleguidance of fine-needle aspiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

drugs that decrease TSH secretion (low serum TSH)

A

DopamineGlucocorticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

drugs that INCREASE thyroid hormone secretion

A

IodineAmiodarone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

drugs that DECREASE thyroid hormone secretion

A

LithiumIodineAmiodarone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

drugs that DECREASE T4 absorption

A

Ferrous Sulfate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

drugs that INCREASE TBG concentration

A

Estrogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Management of Hypothyroidism

A

Lifelong replacement therapyAutoimmune causes - removal or ablation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Drug for Thyroid Replacement Therapy and Goal of Treatment

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Thyroid Replacement for Healthy Patients

A

full dose1.6 ug/kg/dayreassess TSH in 6-8 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Thyroid Replacement in Elderly Patients or those with Cardiac Disease

A

start low and go slow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Signs and Symptoms of Hyperthyroidism

A

GoiterSweating of handsWeight lossTirednessPalpitationsRegular Pulse > 90Lid LagDyspnea on ExertionFinger TremorNervousnessExcessive SweatingHot HandsPreference for ColdExopthalmosHyperkinesisDiarrheaScant MensesAtrial Fibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What is Apathetic Hyperthyroidism?

A

elderly patients present with minimal symptomology of hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Signs and Symptoms of Graves Disease

A

Diffuse Nontoxic GoiterOphthalmopathy: stare, lid lag, exopthalamosDermopathy - pretibial myxedemaThyroid Acropachy - digital clubbing, periosteal reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Causes of Hyperthyroidism

A

GravesToxic Multinodular GoiterThyroid NoduleThyroiditisExogenous intakeMedications: Amiodarone; iodineRARE: adenoma, trophoblastic disease, stuma ovarii

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Complications of Hyperthyroidism

A

Very distressingAtrial FibrillationCHF, Angina, MI, Sudden DeathOsteoporosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Hyperthyroidism Treatments

A

Radioiodine ablative therapySub-total thyroidectomyAntithyroid drugsSymptom treatments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Radioiodine Ablative Therapy

A

most common treatment for Gravesgoal of treatment: Hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Sub-total Thyroidectomy

A

goal: leave enough gland to produce endogenous hormonespare: parathyroid glands, recurrent laryngeal nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Antithyroid Drugs

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Symptomatic Treatment of Hyperthyroidism

A

B-Blockers: tremor and heart rateDiltiazem & Verapamil Clonidine** used until definitive treatment completed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What is Thyroid Storm?

A

Sudden severe exacerbation of thyrotoxicosisoften precipitated by trauma, infection, surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Symptoms of Thyroid Storm

A

feversevere tachycardiadelirium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Treatment of Thyroid Storm

A

antithyroid drugs: PTU or methimazolehigh dose glucocorticoidspotassium iodide to suppress further hormone release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Thyroid Nodule Risks for Malignancy

A

prior radiation< 30 years of age; > 60family history

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Evaluation of Thyroid Nodule

A

TSH, Free T4 and T3Normal TSH: fine needle aspirationBenign: follow clinicallyMalignant: surgical referral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Multinodular Goiter

A

diffuse processidentified on physical examlow risk of malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Subacute Thyroiditis

A

cause: postvirals&s: anterior neck pain; elevated ESRtx: symptomatic - analgesicstypically recover euthyroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Painless Thyroiditis

A

autoimmune - leads to long term hypothyroidismno neck discomfortdecreased uptake of radio iodinepostpartum: w/in 1 year of deliverysilent: not associated w/ childbirth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

FOUR Phases of Thyroiditis

A

HyperthyroidEuthyroidHypothyroidSome recover to a euthyroid state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q
  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

A. B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q
  1. 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

A. Chemotaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q
  1. 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

A. The adaptive immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q
  1. The immunoglobulin that is associated with allergic reactions: A. IgA B. IgD C. IgE D. IgG E. IgM
A

C. IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q
  1. 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
A

C. Epitope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q
  1. 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

A. It actively crosses the placenta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q
  1. 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
A

D. Phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q
  1. The immunoglobulin that is found predominantly in secretions: A. IgA B. IgD C. IgE D. IgG E. IgM
A

A. IgA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q
  1. 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
A

D. T-helper cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q
  1. 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

A. Produced by the liver and circulate in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q
  1. 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
A

B. C3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q
  1. 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

A. Affinity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q
  1. Lysis of cells by complement is finalized by the formation of : A. C1q B. Immune Complexes C. Membrane Attack Complex (MAC) D. Properdin
A

C. Membrane Attack Complex (MAC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q
  1. 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.
A

B. The predominant response is IgG.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q
  1. 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
A

B. Macrophage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q
  1. 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
A

B. Common lymphoid progenitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q
  1. 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
A

E. All of the above

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q
  1. 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
A

B. Is reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q
  1. The class or subclass of an immunoglobulin is determined by the: A. CH region B. CL region C. VH region D. VL region
A

A. CH region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q
  1. Polymorphonuclear granulocytes include: A. B-cells B. Endothelial cells C. Neutrophils D. T-cells
A

C. Neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q
  1. 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.
A

B. Conformational antigens (approximately 125 amino acids).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q
  1. 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
A

D. Undergoes class switching, becomes a plasma cell and secretes an antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q
  1. 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
A

C. Presentation through Class I or Class II molecules that have peptides bound to them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q
  1. 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
A

B. Cilia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q
  1. 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
A

C. Binding to an antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q
  1. 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
A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q
  1. 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
A

B. Before they encounter antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q
  1. 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

A. Can be enhanced by antigen binding to complement or antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q
  1. 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
A

B. Bacteria do not express MHC Class I that is necessary for cytotoxic T cell recognition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q
  1. 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

A. Oncofetal antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q
  1. 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
A

B. Taking out the bone marrow, using antibody to the tumor to remove tumor cells and then putting the remaining cells back in

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q
  1. An example of a known oncogenic virus is: A. Herpes zoster B. HIV-2 C. Epstein-Barr virus D. Vesicular stomatitis virus
A

C. Epstein-Barr virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q
  1. 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
A

B. Cell mediated immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q
  1. Extracellular bacteria are optimally killed by: A. Macrophages B. Complement C. Antibody D. Macrophages plus complement E. Macrophages plus antibody plus complement
A

E. Macrophages plus antibody plus complement

174
Q
  1. 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
A

B. T-cells

175
Q
  1. Cytotoxic T-cells: A. Are usually CD4+ B. Recognize native viral antigen C. Kill virally infected cells D. Kill viruses directly
A

C. Kill virally infected cells

176
Q
  1. Protection against worm infestations is particularly associated with an increase in: A. IgD B. IgE C. IgG D. IgA E. IgM
A

B. IgE

177
Q

T/F: Heavy chains: two for each immunoglobulin molecule and they are identical

A

True- Light chains are identical too but are either Kappa (80%) or Lambda

178
Q

Immunoglobulin gene rearrangement happens in the presence/absence of antigen?

A

Absence

179
Q

T/F: Heavy chains have VJ while light chains have VDJ

A

False

180
Q

_______ Chain rearrangement begins first in the absence of antigen in the primary lymphoid tissues

A

Heavy

181
Q

___ combines with C which most often codes for IgM constant region or IgD.

A

VDJ

182
Q

Once VJ try to combine up to 3 times on the light chain, does the cell die?

A

IgLambda light chain rearrangement occurs only after kappa light chain does not successfully rearrange.

183
Q

T/F: Once rearrangement has occurred successfully, IgM is placed on the cell surface as a receptor?

A

True- Membrane bound, monomer on the cell surface (sIg), becomes pentamer in circulation, when secreted by plasma cell

184
Q

Germ line theory of diversity: (5 parts)

A

1) Multiple genes2) Somatic mutation (only with B cells/presence of antigen)3) Somatic recombination4) Gene conversion5) Recombinatorial imprecision

185
Q

Heavy chain re-arrangement occurs following Ig gene rearrangement in the _________ lymphoid tissue and is have antigen/non-antigen dependent.

A

Secondary, antigen dependent

186
Q

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

A

beta, gamma

187
Q

T cell gene rearrangements occur ___________ for the alpha and beta, or gamma and delta genes

A

Simutaneously

188
Q

B-cells see ___ amino acids while T-cells see a peptide at ~____ amino acids

A

125, 10

189
Q

CD3 molecule is always on what type of cell

A

T cell

190
Q

Anything that starts with “D” is class ____ and everything else (A,B,C) is class ___

A

2, 1

191
Q

CD4 binds:

A

MHC class 2

192
Q

All A, B, or C (class 1) have the same basic structure, differ at the __________ site by the peptides they can bind.

A

Binding- Class 2 looks just like class 1 but has two distinct polypeptide chains

193
Q

Function of Class 1 is to present peptide to the:

A

T cell receptor- So does Class 2

194
Q

MHC class 1 is found on all ________ cells while MHC class II is found on all _____________ cells

A

Nucleated (not RBC), antigen presenting cells (Macrophage, dendritic, B cells)

195
Q

Binding of antibodies to antigens is NOT _____ and follows Michaelis-Menton kinetics

A

STATIC

196
Q

MHC Class II is made in the ________ __________ and the _________ is cleaved into fragments

A

Endoplasmic reticulum, antigen

197
Q

MHC Class I senses inside/outside cell and presents it to the immune system

A

Inside- Made in the endoplasmic reticulum as well just like Class II but the difference is INSIDE the cell

198
Q

Cells altered by chemicals, mutations, and viruses that result in immortalization is what and how do they occur?

A

Tumor: Lose contact inhibition and other growth characteristics thus they do not grow faster, just uncontrolled.

199
Q

Monoclonal comes from ____ cell type

A

one

200
Q

Oilgoclonal comes from multiple cell types, usually up to __

A

8

201
Q

Polyclonal is

A

Multiple cell types usually more than 8

202
Q

What is some evidence immune surveillance exists?

A

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
Q

Tumor associated antigens are ______ and _________.

A

Shared and associated- cross reactivity with tumors of common origin

204
Q

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?

A

No tumor growth- shows tumor specific antigens

205
Q

Example of normal differentiation antigens: CALLA

A

Cellular, Acute, Lymphoblastic, Leukemia, Antigen

206
Q

In tumor, you use CD4, CD8, and what else?

A

Macrophage

207
Q

T cytotoxic cells (CD_+) are capable of killing tumors, but they also need CD_+ T cells for help and direction

A

8, 4

208
Q

T/F: TH1 cells activates macrophages resulting in type IV hypersensitivity where the host is killing the graft (your tumor)

A

True

209
Q

T/F: K or NK cells can release enzymes (Perforin and Granzymes) to lyse the cell without antibody

A

False- need antibody

210
Q

Mechanisms for Tumor to escape Immunosurveilance

A

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
Q

Active, non-specific, immunotherapy for tumors

A

Administering immune-modulators

212
Q

Active, specific, immunotherapy for tumors

A

Therapeutic vaccines of tumor cells, cell extracts, antigens, peptides, proteins, or DNA-pulsed dendritic cells

213
Q

Passive, non-specific, immunotherapy for tumors

A

Lymphokine activated killer cells are activated in vitro and then placed back in host- no specificity

214
Q

Passive, specific, immunotherapy for tumors

A

Antibodies alone or coupled to drugs,etc

215
Q

Antibiotic Mechanisms - sulfonamides

A

competitive antagonism

216
Q

Antibiotic Mechanisms - penicillins

A

cell wall inhibition

217
Q

Antibiotic Mechanisms - antifungals

A

cell membrane interference

218
Q

Antibiotic Mechanisms - erythromycin

A

protein synthesis inhibition

219
Q

Antibiotic Mechanisms - tobramycin

A

protein synthesis alteration

220
Q

Antibiotic Mechanisms - ciprofloxacin

A

nucleic acid interference

221
Q

Penicillins

A

Beta-lactam antibioticsLow toxicityCross-allergenicityG+ coccal infections

222
Q

IM Penicillins

A

Procaine & Benzathine or combinationcreate low blood levels of drug - used for syphilis

223
Q

Ampicillin/Amoxicillin

A

Penicillin coverage + H. flu + e.coliused: oral, sinus, skin infectionproblems: diarrhea, allergy, maculopapular rash

224
Q

Amoxicillin/Potassium Clavulanate (Augmentin)

A

fixed dose amoxicillin combination with B-lactamase inhibitorside effects: GI upset, diarrhea

225
Q

Penicillinase-Resistant Penicillins (2)

A

OxacillinDicloxacillin

226
Q

1st Generation Cephalosporins

A

gram-positive cocciCefazolin, Cephalexin, Cefadroxil

227
Q

2nd Generation Cephalosporins

A

gram-positive cocci, some gram-negative, some anaerobesCefuroxime, Cefoxitin

228
Q

3rd Generation Cephalosporins

A

gram-positive cocci, > gram-negative spectrum can penetrate CSFCefotaxime, Ceftriaxone, Ceftazidime

229
Q

4th Generation Cephalosporins

A

gram-positive, increased activity versus enterobacteriacea, pseudomonas

230
Q

Macrolides - Erythromycin uses

A

penicillin substitute for Mycoplasma, Chlamydia, or campylobacter

231
Q

Macrolides - Azithromycin

A

more gram-negative coverage than erythromycin

232
Q

Macrolides - Clarithromycin

A

used is AIDs related infections; H. pylori eradication

233
Q

Ketolide

A

Telithromycin - macrolide derivativecommunity acquired pneumonias > 18 liver & other toxicities

234
Q

Tetracyclines

A

Gram-negative rods, rickettsial, chlamydia, lyme disease, acne, penicillin-resistant G+ infectionstetracycline, doxycycline, minocycline

235
Q

Tetracyclines Contraindications & Side Effects

A

AVOID in pregnancyGI upset, tooth staining, vertigo

236
Q

Clindamycin

A

aerobic gram-positive cocciproblem: C. difficile overgrowth

237
Q

Vancomycin

A

used for MRSA, staph epidermidis

238
Q

Fluoroquinolones

A

DNA gyrase inhibitorsgram negative rods & cocci, psuedomonas, gram positiveCiprofloxacin, Ofloxacin, Levofloxacin, Moxifloxacin

239
Q

Sulfonamide Toxicities

A

allergic reactionsblood dyscrasias

240
Q

Metronidazole Use

A

used against anaerobes of GI origin, giardia, bacterial, trichomonal vaginal infections

241
Q

Metronidazole Toxicities

A

nausea, headache, metallic taste, disulfiram-like reaction with alcohol

242
Q

Antibiotics and Oral Contraceptives

A

amoxicillin, metronidazole and tetracyclines - interfere with oral contraceptive efficacy

243
Q

T/F: Viruses do not replicate without host machinery?

A

True

244
Q

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.

A

True

245
Q

Internal antigens of a virus. Mainly the ____________, but antibodies to internal antigens are protective/non-protective?

A

Nucleocapsid, non-protective

246
Q

Viruses selectively destroy and affect certain tissues because:

A

Attachment is through the specific receptors

247
Q

Small viruses “slipping” through the membrane by chance and hydrophobicity is called what?

A

Viropexis penetration

248
Q

Most viruses enter cells in this way:

A

Receptor mediated endocytosis

249
Q

T/F: Uncoating occurs in the nucleus by enzymes or through phagolysosomal granules

A

False: occurs in cytoplasm

250
Q

Replication of viruses: DNA viruses replicate in the ________

A

Nucleus- but both RNA and DNA make protein through mRNA

251
Q

Replication of viruses: RNA viruses replicate in the ________

A

cytoplasm- but both RNA and DNA make protein through mRNA

252
Q

Immunity to viruses is primarily __ Cell mediated. Explain:

A

T-cell: Class I restricted cytotoxic cells as all nucleated cells have MHC class I.

253
Q

T/F: In virus infections, you can have Non-neutralizing and neutralizing antibodies?

A

True- Hopefully you have neutralizing antibodies

254
Q

Interferon (IFN) alpha and beta do what?

A

Are released by virally infected cells to the surrounding cells. Have the capability of inhibiting viral infection of the uninfected cells.

255
Q

Interferon-gamma causes increased __________

A

Responsiveness

256
Q

T/F: Bacteria have their own MHC Class I and MHC class II

A

False

257
Q

Catalase is 1 way bacteria escape phagocytosis. What does catalase break down?

A

Hydrogen peroxide

258
Q

If you have a bacterial abscess and cut it open, what 4 things would you most likely see from bacterial immunity?

A

Antibody, macrophages, neutrophils, complement. Mediated by CD4 T helper cells.

259
Q

Immunity to fungi: Primarily cell mediated through:

A

MHC Class I and Class II- probably through some antigen presentation through dendritic cells

260
Q

Important cells in parasite immunity:

A

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
Q

Fever CriteriaRectal:Oral:Axillary:

A

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
Q

Fever Without a Source

A

children with a fever lasting for one week or less without adequate explanation after a careful history and thorough physical examination

263
Q

Fever of Unknown Origin

A

fever > 101 F of at least 8 days durationno diagnosis apparent after initial outpatient or hospital evaluation

264
Q

All babies 3 months or younger with a fever of 100.4 or higher MUST

A

BE SEEN THAT SAME DAY!

265
Q

Fever in Infants < 3 months: Bacterial S&S

A

bacterial infectionss&s: low grade fever, poor feeding, irritability, sleepiness/sleeplessness

266
Q

Fever in Infants < 3 months: History

A

Associated Symptoms: respiratory, GI, ENTBehavioral Symptoms: poor feeding, irritability, poor sleeping, abnormal cryExposure to Sick Contacts: siblings, babysitter, day carePrevious IllnessBirth History

267
Q

Fever in Infants < 3 months: Physical Exam

A

GestaltAbnormal Vital SignsToxic AppearanceSigns of Localized Infection

268
Q

Toxic Appearance

A

irritabilityinconsolabilitypoor perfusionpoor tonedecreased activitylethargy

269
Q

Common Pathogens < 3 months - Bacteremia

A

S. pneumoniaeHibgroup B strepN. meningitissalmonellaListeria monocytogenes

270
Q

Common Pathogens < 3 months - UTI

A

E. coli

271
Q

Common Pathogens < 3 months - Pneumonia

A

S. aureusS. pneumoniaegroup B strep

272
Q

Common Pathogens < 3 months - Meningitis

A

S. pneumoniaeHibgroup B strepmeningococcusherpes simplexenterovirus

273
Q

Sepsis Evaluation

A

CBC w/ differentialSerum GlucoseLumbar PunctureBlood CultureUrine CultureInflammation Indicators: ESR, CRP, ProcalcitioninConsider: stool culture, CXR

274
Q

When to admit fever in infant < 3 months for empiric antibiotics? (3)

A

Toxic Looking< 1 month of agePoor social situation

275
Q

Outpatient Observation Fever < 3 months

A

Option 1: blood culture, urine culture, lumbar puncture - Ceftriaxone - re-evaluate in 24 hoursOption 2: urine culture, careful observation

276
Q

Fever in Children < 3 years

A

most illness in this age group are self-limited viral infectionsincreased risk of occult bacteremia

277
Q

Common Pathogens for Fever in Children < 3 years

A

S. pneumoniaeHibN. meningitisnon-typhoidal SalmonellaUTI and pneumonia are possible causes of occult infection

278
Q

Fever in Children < 3 years - History

A

Functional Status: oral intake, activity level, irritabilityCough, Vomiting, Dysuria, Frequency, Potty AccidentsImmunization Status!!!!

279
Q

Physical Exam Children 3-36 Months - Findings warranting extra attention

A

Toxic AppearingCyanosisHypo/HypervenilationAbnormal Vital Signs - SpO2 < 95%TachycardiaTachypneaLesions in OropharynxAbdominal TendernessPain with bone palpation or passive ROMPetechiae, cellulitis, viral exanthem

280
Q

Gestalts in feverish children < 3 years

A

AlertnessPlayfulnessIrritabilityConsolability

281
Q

Risk Factors for Occult Bacteremia

A

Temp > 102.2 FWBC > 15,000/mm3Elevated neutrophils or bandsElevated ESR, CRP or PCT

282
Q

What type of fever has:high spike and rapid resolution

A

Intermittent FeverTB, lymphoma, JIA/JRA

283
Q

What type of fever has:fluctuant peaks, but doesn’t return to normal

A

Remittent Feverviral, endocarditis, sarcoid, lymphoma, atrial myxoma

284
Q

What type of fever has:fever persists with little fluctuation (unless meds given)

A

Sustained Fevertyphoid fever, typhus, brucellosis

285
Q

What type of fever has:fevers that relapse after 1 or more days with no fever

A

Relapsing FeverMalaria, rat-bite fever, Borrelia infection, lymphoma

286
Q

What type of fever has:episodes of fever more than 6 months duration

A

Recurrent Feverother causes: metabolic defects, CNS abnormalities, immunodeficiency

287
Q

Fever of Unknown Origin

A

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
Q

Fever of Unknown Origin - Skin Examination

A

presence of sweatingpetechiaerashsparse hair

289
Q

Fever of Unknown Origin - Eye Examination

A

ConjunctivitisRetinopathyAbsence of pupillary responseAbsent tears or corneal reflexesAbnormal fundoscopic exam

290
Q

Fever of Unknown Origin - Oropharynx Examination

A

Hyperemia of posterior pharynxDental abscessAbnormal DentitionSmooth tongueGinigival Hypertrophy

291
Q

Fever of Unknown Origin - Lymph Node Examination

A

Enlarged and/ore multiple lymph nodes

292
Q

Fever of Unknown Origin - Chest Examination

A

CracklesNew onset murmur

293
Q

Fever of Unknown Origin - Abdomen Examination

A

OrganomegalyTenderness with liver palpation

294
Q

Fever of Unknown Origin - Musculoskeletal

A

Tenderness to bones or musclesHyperactive DTRs

295
Q

Fever of Unknown Origin - GU

A

STD testingCareful exam for any masses or abscessesStool should be examined for occult blood

296
Q

An antibody to an Antigen is known as an immune what?

A

Complex

297
Q

With the classical complement pathway, you need what to activate it?

A

Antibody binds to antigen

298
Q

What activates C3 in the alternative pathway?

A

H2O

299
Q

C3 convertase in classical pathway? C3 convertase in alternative pathway?

A

Classical= C4b2aAlt=C3bBb

300
Q

Ultimately, the complement pathway ends by doing what to the cell?

A

Lysis by MAC attack

301
Q

T/F: C5 activates adhesion molecules on macrophages?

A

True

302
Q

What cell controls other cells (macrophage, granulocyte, NK cell,etc. or in Thiele’s terms, is the “mother” of all cells?

A

T-Helper cells

303
Q

T-Cytotoxic cells are important in recognition and killing by what mechanism?

A

Granules: Lyse (perforin) and enzymes

304
Q

T helper cells: CD4 or CD8? Sees how many amino acids?

A

CD4+, CD4 binds MHC class II, looks for peptide in groove and sees 8-14 amino acids

305
Q

T cytotoxic cell: CD4 or CD8 and sees how many amino acids?

A

CD8+, CD8 binds MHC class I and looks for peptide in groove. Sees 8-14 amino acids. On all nucleated cells!!

306
Q

What are B cells?

A

Surface Immunoglobulin (sIg)= receptor for an epitope on an antigen. Also an antigen presenting cell. Sees 125 amino acids

307
Q

Linked recognition means what?

A

Process by which a TCR and a sIg recognize different epitopes on the same antigen, thus linking their response

308
Q

If you perform a transplant, you want to knock out what?

A

CD4

309
Q

T/F: Overweight at age 4=20% chance in adulthood.

A

True

310
Q

BMI Standards for Overweight, Obese (Class I and II), and Morbidly obese

A

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
Q

Children BMI percentile ranges

A

-BMI between 85-95th%ile = At risk for obesity-BMI>95th%ile = Obese

312
Q

Obesity patterns: Android

A

Truncal Obesity= Increased incidence of morbidity and mortality

313
Q

Obesity Patterns: Gynecoid

A

Hip/Gluteal obesity

314
Q

Other measures than BMI for Obesity

A

-Waist-to-hip ratio: >1.0 males and >0.85 females-Abdominal Circumference: >102cm males and >88cm females

315
Q

What is most basic cause of Obesity?

A

Calories in vs. calories out= energy intake exceeds energy use.

316
Q

Some multifactorial causes of obesity:

A

1) Genetics (Leptin, etc.) with interaction of environment.2) Environmental (Sleep, smoking cessation, social, dietary factors, etc.)3) Endocrine4) Medications5) Psychological

317
Q

Prenatal Influences on obesity:

A

-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
Q

Neuroendocrine Causes of Obesity

A

Cushings Syndrome, Hypothyroidism, Polycystic Ovary Syndrome, Growth hormone deficiency, “Hypothalamic obesity”-Signs for women may be Hirsutism

319
Q

A congenital etiology of obesity

A

Prader-Willi Syndrome

320
Q

List some Comorbidities of obesity

A

Metabolic syndrome, Insulin resistance, DM II, HTN, CV disease, Dyslipidemia, Respiratory problems, Sleep apnea, hernias, reflux, stress incontinence, hemorrhoids, skin problems, psychologic.

321
Q

Associated comorbidities of Obesity

A

-Venous problems, Increased risk of cancer, GI problems

322
Q

Acanthosis nigricans is a sig of elevated _________ levels

A

Insulin. Early insulin resistance and DM II

323
Q

1st line Treatment for an adult with Obesity

A
  • 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
Q

2nd line Treatment for an adult with Obesity (Classes of Medications)

A

-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
Q

Sympathomimetic (Catecholaminergic) medictions for obesity

A

1) Phentermine (Fastin)- stimulant2) Sibutramine (Meridia)

326
Q

Drugs that alter digestion for Obesity

A

1) Orlistat- Decrease fat absorption (OTC is Alli)

327
Q

Serotonin Agonists for Obesity

A

-Loracaserin-Fluoxetine (Prozac) and Bupropion (Wellbutrin)

328
Q

Surgical treatment for Obesity and requirements.

A
  • 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
Q

What should be present with all treatment options in obese patients?

A

Behavioral therapy- Alter eating and physical activity habits

330
Q

Beta-lactams are effective against Gram +/ Gram Negative?

A

Gram Positive

331
Q

Beta Lactams bind

A

penicillin binding proteins blocking cross linking causing cell death

332
Q

MRSA has altered Penicillin Binding protein and decreased affinity for all B-lactams. This was likely acquired from:

A

Coag-negative Staph

333
Q

Vancomycin binds to

A

Cell wall precursors

334
Q

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?

A

True

335
Q

T/F: VRSA was first seen in 2002 with few reports and all the organisms contained the vanB gene?

A

False: contained vanA

336
Q

Which of the following does not have activity against MRSA?A) BactrimB)ClindamycinC) ErtapenemD) LinezolidE) Tigecycline

A

C) Ertapenem- B-lactam drug

337
Q

Treatment for S. Aureus skin and soft tissue infections:A) For a boilB) MSSAC) MRSA

A

A) Surgical drainage- usually adequateB) Oxacillin/NafcillinC) Vanco, Linezolid, Daptomycin, Tigecycline

338
Q

What antibiotic causes C. difficile?

A

Clindamycin

339
Q

T/F: Linezolid is superior to vancomycin for treating MRSA pneumonia

A

False: Equivalent

340
Q

Therapy for MRSA pneumonia

A

Start with Vancomycin, then linezolid. Do not use Daptomycin (inactivated by surfactant)

341
Q

Therapy for MRSA Bacteremia

A

Start with Vancomycin, then Daptomycin

342
Q

What are 3 mechanisms that decrease permeability in gram negative organisms?

A

1) Decreased porin expression2) Active efflux pumps3) Multi-drug efflux pumps

343
Q

Definition of multidrug-resistant

A

Resist at least one agent in 3 or more classes

344
Q

What class of drugs was created to overcome Beta-lactamases?

A

3rd generation cephalosporins

345
Q

4 risk factors for extended spectrum Beta lactamases (ESBL) are:

A

Location, Antibiotic use, Severity of illness, Devices

346
Q

Clinical presentations of ESBL infections:

A

UTI, Wound infections, pneumonia, intra-abdominal infections

347
Q

Which of the following is the drug of choice for severe ESBL producing organism infections?A) FQB) TMP/SMXC) CefepimeD) Piperacillin/tazobactamE) Carbapenems

A

E) Carbapenems

348
Q

T/F: You can use cephalosporins for ESBL treatment

A

False. DO NOT USE!

349
Q

Carbapenamases hydrolyze all:

A

Beta-lactams

350
Q

What can make Klebsiella pneumoniae and E.coli highly resistant to almost every drug?

A

NDM-1: New Delhi Metallo-beta-lactmase 1

351
Q

Treatment for Carbapenemase Producers

A

No beta lactams. Colistin (nephrotoxic, neurotoxic)? Tigecycline (increased mortality)?

352
Q

Mutation in DNA gyrase and/or topoisomerase IV are alteration in enzymes leading to what type of resistance?

A

Quinolone resistance in gram-negative pathogens

353
Q

Endocrine vs. Exocrine

A

ENDO is hormones secreted internally and EXO is secreted externally or into the lumen

354
Q

Palpable endocrine glands

A

Thyroid, Gonads

355
Q

Primary evaluation of the endocrine system is:

A

Measuring hormone concentrations

356
Q

Functions of hormones (3)

A

Growth, Maintenance of homeostasis, reproduction

357
Q

Presentation of Cushing Syndrome

A

Central fat redistribution, striae, proximal muscle weakness, hirsutism, elevated BP, increased BMI, “buffalo Hump”

358
Q

What is it? Lethargy, weakness, psychomotor retardation, cold intolerance, constipation, hair loss, dry skin, and weight gain

A

Presentation of hypothyroidism

359
Q

Appropriate screening for hypothyroidism

A

TSH, confirm free T4

360
Q

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

A

Addison Disease

361
Q

What is it? 22 y.o. women with breast secretions, amenorrhea, and decreased libido, BP=140/80, no other symptoms or abnormalities

A

Hyperprolactinemia most likely from a benign (posterior) pituitary tumor

362
Q

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

A

False: Must be confirmed on another day by any one of the criteria

363
Q

Diagnostic criteria for DM type II

A

-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
Q

Tests NOT used in initial diagnosis of DM II

A

Insulin levels, C-peptide levels, screening for autoantibodies

365
Q

Prediabetes criteria and what does this mean

A

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
Q

Metabolic syndrome criteria

A

Insulin resistanceHypertensionDyslipidemia (Trigs >150 or HDL-C<40)Abdominal obesity

367
Q

Fasting glucose levels that indicate significant beta cell failure

A

200 mg/dL

368
Q

In treatment of DM II you should always start with what?

A

Therapeutic Lifestyle Modification

369
Q

Patients with FPG < 250 mg/dL should be treated how

A
  • Medical nutritional therapy, exercise program. If not controlled in 3 months, move to next step
370
Q

Patients with FLG > 250 but <400 mg/dL who do not have signs of dehydration, acidosis or marked ketosis

A

In addition to medical nutritional therapy, begin monotherapy with an oral antidiabetic agent (metformin)

371
Q

T/F: Patients with marked elevated FPG and ketonuria or ketonemia or symptomatic patients may require require insulin therapy initially to overcome glucose toxicity?

A

True

372
Q

What is considered best first line agent for DM II?

A

Metformin

373
Q

Do not use or use metformin cautiously in what patients?

A

Do not use in Pts prone to lactic acidosis, if serum creatine is elevated, use cautiously in renal and hepatic disease

374
Q

If blood glucose is severely elevated, you should use what therapy

A

Sulfonylureas (Glyburide, Glipizide)- May be 1st choice in lean persons who have more pancreatic dysfunction than insulin resistance

375
Q

a-glucosidase inhibitors are most effective in persons with

A

Mild fasting hyperglycemia, predominantly postprandial hyperglycemia

376
Q

An agent used in adjunct to oral agents (Metformin and/or sulfonylureas) that is given as SQ injection and is an Incretin mimetic

A

Exenatide/ Liraglutide

377
Q

Shin spots are:

A

Pigmented atrophic macular areas on the skin over the tibia frequently seen in diabetic patients

378
Q

Necrobiosis Lipoidica is:

A

Cutaneous sign associated with DM, an irregular erythematous patch, occurs anywhere on the legs, 2-10cm

379
Q

Inability to perceive monofilament indicates

A

Advanced neuropathy

380
Q

Medical management of Diabetic neuropathy

A

-Specific: Duloxetine (Cymbalta)-Gabapentin, Amitriptyline, other neurostabilizers (Carbamazepine), Analgesics (NSAID, Acetaminophen)

381
Q

Onset of nonproliferative retinopathy is indicated by:

A

Microaneurysms (early findings). Proliferative retinopathy with neovascularization/hemorrhages

382
Q

Diabetic patients with BP over what needs medication

A

135/85- ADA recommends lowering BP to 130/80 mmHg or less

383
Q

Diabetics with LDL greater than what need lipid lowering therapy

A

130 mg/dL- Target LDL is 100, maybe even as low as 70

384
Q

Emergency complications of DM (3)

A

1) Diabetic ketoacidosis2) Nonkinetic hyperosmolality syndrome3) Hypoglycemia (insulin reaction)

385
Q

Etiology of Dm type 1

A

-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
Q

What is the most common pediatric endocrine disorder?

A

DM1

387
Q

Some symptoms of DM1

A

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
Q

Presentation of DKA

A

Polyuria, Polydipsia, nausea, vomiting, abdominal pain, tachypnea, fruity odor to breath

389
Q

A 12 year old female with DKA. What potential side effect do you want to avoid with treatment?

A

Cerebral edema- get an endocrinologist involved

390
Q

How to treat dehydration in a DM1 patient

A

glucose free isotonic solution

391
Q

How to correct hyperglycemia

A

Fast acting insulin (decrease at 100mg/dl/hr)

392
Q

How to treat acidosis

A

Should be corrected with insulin- bicarb only in severe cases

393
Q

How to treat electrolyte imbalance

A

Potassium needs to be replaced

394
Q

Therapy for DM1: Usual starting dose of insulin

A

0.5U/kg: 50% given to provide basal coverage, 50% divided doses for rapid acting insulins

395
Q

Long acting insulins

A

Used for basal coverage: Insulin glargine (Lantus), Insulin detimir (Levemir). Not used in pump

396
Q

Rapid acting synthetic insulin

A

Insulin lispro (Humalog), Insulin aspart (Novolog), Insulin glulisine (Apidra). Completely gone within 3 hours, used in pumps

397
Q

Hypoglycemia results from an ______ of insulin in relation to the serum glucose concentration. Symptoms include: and the Treatment is:

A

Excess.Symptoms: Headache, visual changes, confusion, irritability, seizures, tremors, tachycardia, diaphoresis, anxiety.Treatment: Fast acting glucose- glucose tabs, soda, juice

398
Q

Goal for A1c in a DM1 patient

A

<7.0%

399
Q

DM1 phenomena: Honeymoon period

A

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
Q

Somogyi Phenomenon

A

Early morning hyperglycemia that is actually caused by hypoglycemia at night.

401
Q

Dawn Phenomenon

A

Early morning hyperglycemia caused by early dosing of evening insulin and secretion of GH in early morning hours

402
Q

DM1 preventative care

A

-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
Q

Decrease in C-peptide plus diabetic symptoms is what type of diabetes?

A

Type 1

404
Q

Normal C-peptide plus symptoms is what type of diabetes

A

Type 2

405
Q

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

A

Less than 7.25, <15mEq/L, Elevated

406
Q

Syndrome X and Insulin resistance is also known as

A

Metabolic Syndrome

407
Q

Risk Factors for Metabolic syndrome

A

Abdominal obesity (M=40, F=35)Elevated BP (130/85)Elevated Triglycerides ( >150)Elevated FBG (>110)Low HDL (Males<50)

408
Q

T/F: Patients with Metabolic syndrome are typically symptomatic before complications occur

A

False: Typically asymptomatic until they develop 1 or more complications (Ex: BP>130/85, Abdominal obesity)

409
Q

Diagnostic criteria for Metabolic Syndrome

A

If 3 risk factors are presentAbdominal obesity (M=40in, F=35in)Elevated BP (130/85)Elevated Triglycerides ( >150)Elevated FBG (>110)Low HDL

410
Q

Supporting lab tests for Metabolic Syndrome

A

Abnormal liver fxnIncreased CRPIncreased Uric acidMicroalbuminIncreased serum testosterone in women May be appropriate to order: Cardiac stress test, carotid US, Coronary Calcium scoring

411
Q

What are therapeutic life changes (TLC) for Met. Syndrome

A

Weight loss (Mediterranean Diet)Dietary modificationsIncrease aerobic exercise (30 min daily)

412
Q

Along with weight loss, balanced diet, and exercise, what other therapy should you give a patient with Metabolic Syndrome to prevent DMII?

A

Metformin

413
Q

MetS: Treatment for cardiac risk factors:

A

-HMG-CoA reductase inhibitors (Statin)-Gemfibrozil-Diet, exercise, weight loss

414
Q

Treatment for Obesity

A

Bariatric surgeryOrlistat, Sibutramine

415
Q

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?

A

Metabolic Syndrome

416
Q

Leading cause of death in the US?

A

Cardiovascular Disease (CVD)- associated with high cholesterol and lipids with decreased HDL

417
Q

NCEP ATP III risk determinants for CHD: HDL

A

Optimal: >60Borderline High 40-59High Risk >40

418
Q

NCEP ATP III risk Categories

A

-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
Q

T/F: A very high risk patient for CHD has LDL >100. Should you consider drug therapy?

A

Yes

420
Q

You have a moderate high risk patient with LDL <130, should you start therapy?

A

It is optional. >130 start therapy.

421
Q

When do you start therapy for moderate risk patient for CHD

A

LDL >160

422
Q

Low risk patient for CHD. When should you start therapy?

A

LDL >190

423
Q

High risk patients with high TG or low HDL levels what should you consider?

A

Fibrate or nicotinic acid

424
Q

Pattern of Dyslipidemia in DMII patients

A

High trigs, low HDL, Qualitative changes in LDL

425
Q

Patient with diabetes should get their LDL below what

A

<100 without CVD

426
Q

Fibrate can do what to your trigs and HDl levels

A

Decrease Trigs, increase HDL

427
Q

Niacin (nicotinic acid) can do what to trigs and HDL levels?

A

Decrease trigs, increase HDL- can cause flushing

428
Q

Ezetimibe (Zetia) can do what?

A

Further decrease LDL levels by selectively inhibiting intestinal absorption of cholesterol

429
Q

Bile acid sequestrants may do what

A

Decrease LDL

430
Q

What is lifestyle changes dont decrease lipid levels? What should you prescribe next

A

Statin- follow up in 6wk to check labs. No improvement, increase dose

Adult/Ped Medicine Cumulative Final (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions