Test 2 Study Guide Flashcards
How do our bodies identify immune cells?
identified by a specific protein on its cell surface called the
Cluster of Differentiation/CD marker
What is the antigen receptor of the B Cell called?
B Cell Receptor (BCR)
A fully differentiated B cell is called a ______
plasma cell
The presence of C19 or C20 indicate the Prescence of
B Cells
The presence of C3+ indicate the Prescence of
T cells
The presence of CD56+ indicate the Prescence of
Natural Killer Cells (part of innate immunity)
What is the name of the Natural Killer Cell’s receptor?
Killer Inhibitory Receptor
The presence of CD11c+ indicate the Prescence of
Dendritic cells
Another word for WBCs is
Granulocytes
What WBCs can be identified by the presence of CD66b+
◦ Neutrophils
◦ Eosinophils
◦ Basophils
◦ Mast Cells
Neutrophils play a major role in fighting off bacterial infections; eosinophils play a major role in fighting off parasites; and basophils and mast cells play a major role in allergic reactions.
The Prescence of purulence in a wound indicates the presence of which WBC
Neutrophils
Describe the process of phagocytosis in a neutrophil
Bacterium surface antigens connect to neutrophil membrane receptor and neutrophil engulfs bacterium. Bacterium becomes surrounded by a phagosome. Granules (azurophilic, specific) increase PH inside phagosome. A lysosome attaches to the phagosome, becoming a phagolysosome. The phagolysosome digests the contents of the phagosome. The neutrophil dies and is phagocytized by a macrophage.
Which WBC deals with parasites?
Eosinophils
What do basophils do
promote allergic responses
What does the presence of CD14+ indicate?
Presence of monocytes (baby macrophages) or macrophages
Neutrophils make up what percentage of WBC
50-62%
Lymphocytes make up what percentage of WBC
25%–40%
monocytes (baby macrophages) make up what percentage of WBC
3%–7%
Eosinophils make up what percentage of WBC
0%–3%
Basophils make up what percentage of WBC
0%–1%
How long does it take for the adaptive immune system to become effective?
About 4 days
How do our immune cells know how to differentiate between self and pathogens?
PAMPs (Pathogen Associated Molecular Patterns) Ex: flagella, single stranded DNA/double stranded RNA, Chemicals in the walls of fungi
What are the seven aspects of innate immunity
physical/mechanical/chemical barriers
Phagocytosis
Inflammation
acute phase response
fever (pyrexia)
NK cells/antiviral immunity
plasma protein systems
IGG
MOST ABUNDANT ACCOUNTS FOR MOST OF PROTECTIVE IMMUNITY
IGM
LARGEST, FIRST ANTIGEN PRODUCED AT INITIAL RESPONSE
IGD
IgD is a B cell antigen receptor that may participate in B cell maturation, maintenance, activation, and silencing
IGE
USUAALY IN LOW CONCENTRATIONS AND HAS SPECIALIZED FUNCTION IN ALLERGIC REACTIONS
IGA
PROTECTS MUCOSAL SURFACES
MAJOR HISTOCOMPATIBILITY COMPLEX
MHC ENCODES PROTIENS FOR CELL SURFACES SO THAT IMMUNE CELLS CAN RECOGNIZE SELF VS NONSELF
Glycoproteins on the surface of all human cells (except
RBCs)
MAKES HISTOCOMPATIBILTY (COEXISTING TISSUES) POSSIBLE
How bacteria evade our immune system/develop antibiotic
resistance
Coating to evade phagocytes
Degrade complement and IgA
Toxins
Molecular mimicry
Antibiotic resistance
Biofilm
Change antigens
Antigenic Drift
More gradual mutations of surface antigens
Antigenic Shift
Major shifts in genetic recombination, usually in species jumping
Causes of infection
- Virus
- Bacteria
- Fungi
- Protozoa
- Helminths
DIFFERENCE BETWEEN BACTERIOCIDAL AND BACTERIOSTATIC
Bactericidal = kill
Bacteriostatic = suppress
how antibiotics work
ANITBIOTICS DISRUPT:
Bacterial cell wall (structure/protoplasm)
Bacterial protein synthesis (ribosomes)
Bacterial DNA/RNA (nucleic acid/enzymes)
Bacterial enzymes (folic acid synthesis)
2 EXAMPLES OF BACTERIOSTATIC MEDS (INHIBITS PROTEIN SYNTHESIS)
TETRACYCLINES ( Therapeutic Uses: Acne, periodontal disease), MACROLIDES ( Therapeutic Uses
Substitute in PCN allergy)
EXAMPLES OF BACTERICIDAL MEDS (INHIBITS PROTEIN SYNTHESIS)
Aminoglycosides
Therapeutic Uses
Narrow spectrum; Serious infections; aerobic gram (-)
bacilli
WHAT ANTIBIOTIC DISRUPTS THE BACTERIAL CELL WALL
Penicillins
Therapeutic Uses
Primarily Gram (+); broad and
narrow spectrum
Contraindications
Caution with Renal dysfunction
PCN blood levels
Severe PCN allergy
Cephalosporins
(Ceph)
Therapeutic Uses
Primarily Gram (+), multiple
generations
Contraindications
Severe PCN allergy
Adverse effects
Bleeding
Monitor; use caution with pts
on anticoagulants
Thrombophlebitis
WHAT ANTIBIOTIC DISRUPTS THE BACTERIAL METABOLITES
Sulfanomides &
Trimethoprim - Bacteriostatic
Therapeutic Uses
Urinary tract infection
Combination TMP/SMZ more powerfuL
WHAT ANTIBIOTIC DISRUPTS THE BACTERIAL DNA/RNA SYNTHESIS
Fluoroquinolones (Cipro)
Therapeutic Uses
Broad-spectrum; wide varietY
Four Classes of Antifungal Drugs
- Polyene antibiotics
- Azoles
- Echinocandins
- Pyrimidine analogs
General Adaptation Syndrome (GAS)
What triggers a stress response and signs and symptoms
- Stressor triggers the hypothalamic-pituitary-adrenal
(HPA) axis - Activates sympathetic nervous system
- Arousal of body defenses
How the Sympathetic Nervous System (SNS) responds to stress
tHE BRAIN RELEASE acth AND NERVE SIGNALS TO THE ADRENAL GLAND (CORTEX SECRETES GLUCOCORTICOIDS/CORTISOL)(MEDULLA SECRETES ADRENALINE/EPINEPHRINE)
CORTISOL MAKES THE LIVER RELEASE MORE GLUCOSE
ADRENALINE INCREASES HR, BREATHING RATE, BG
α-adrenergic receptors
ALPHA 1 RECEPTORS: AFFECTS SMOOTH MUSCLE ALPHA CONTRACTION (AC) STIMULATE
APLHA 2 RECEPTORS: ON NERVE TERMINALS AND DECREASE NORENIPHRINE RELEASE
INHIBIT
β-adrenergic receptors
β1: HEART & JUXTAGLOMERULAR STIMULATE
β2: AFFECTS SMOOTH MUSCLE ALPHA relaxation (AC) INHIBIT
difference between primary and secondary immunodeficiency
- Primary (congenital) immunodeficiency
– Genetic anomaly
MAJOR CONCEPTS
1. Main symptom is recurring infections.
2. Types of infections indicate immune defect.
3. Family history is important for diagnosis
- Secondary (acquired) immunodeficiency
– Caused by another illness
– More common - Far more common than primary deficiencies
whats meds make it so hiv cant spread
entry/fusion inhibitors
also reverse transcriptase inhibitors, protease (enzyme used to enter t cells) inhibitors, and integrase (enzyme that integrates HIV genetic info with t cell’s) inhibitors
HAR is combo of therapies listed above
stages of hiv
Acute stage: This is the period immediately following exposure, at which time the immune system activates to fight the invaders. Serologically negative
Chronic stage: This is a prolonged period of years and even decades during which the virus gradually depletes CD4 T-cells, often with few notable symptoms. serologically positive but asymptomatic
AIDS: This is the most advanced stage of HIV. Means you have at least two comorbidities that are killing you from having no immune system
What is the window period for the HIV test
What is the window period for the HIV test I took? Antibody tests can usually detect HIV 23 to 90 days after exposure. Most rapid tests and self-tests are antibody tests. A rapid antigen/antibody test done with blood from a finger stick can usually detect HIV 18 to 90 days after exposure
What does the level of Th cells have to be to be diagnosed with AIDs
<200 cells/mm3
What the overall treatment goal and what the goal CD4 T-cell counts are (the
number in cells/mm3) for effective treatment
For HIV infection the goal is to have >500 cells/mm^3, with effective ART (healthy
individuals have 800-1200 cells/mm^3)
organ specific autoimmune diseases
type 1 diabetes mellitus
goodpastures syndrome
multiple sclerosis
graves disease
Hashimoto’s thyroiditis
autoimmunehymolytic anemia
autoimmune addisons disease
vitiligo
myasthenia gravis
systemic autoimmune diseases
rheumatoid arthritis, scleroderma, lupus, Sjogren’s, polymyositis
