2450 wk 3 Flashcards

1
Q

infection

A

invader overwhelms the body’s defenses; may not be clinically apparent

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2
Q

colonization

A

overgrowth of organisms in a body site: sometimes used interchangeably with infection, but not overwhelming to body

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3
Q

describe and name 3 opportunistic pathogens

A

normally found in host or environement, do not normally cause dz, exploit break in host defenses (candida, staph, pseudomonas)

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4
Q

6 links in chain of infx

A
  1. infx agent
  2. reservoir
  3. portal of exit
  4. transmission
  5. portal of entry
  6. host
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5
Q

define vertical transmission & name 3 types & effects

A

mother to baby
tranplacental, transcervical, breastfeeding
mental retardation, blindness, deafness

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6
Q

vertical transmission (TORCH)

A
Toxoplasmosis
Other (HIV syphilis gonorrhea)
rubella
cytomegalovirus
herpex simplex
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7
Q

3 methods of infx diagnosis

A

1 clinical evidence (systematic complaints, vital signs)

  1. labs
  2. urinanalysis
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8
Q

5 lab values that indicate infx

A
  1. wbc
  2. esr
  3. crp
  4. culture
  5. serology (used for titers, to ID antigens, and when culture is not possible)
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9
Q

purpose of U/A

A

screening for infx, renal funx, fluid balance

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10
Q

U/A test results that indicate UTI

A

visual: cloudy, amber
chemical: nitrite, leukocyte esterase

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11
Q

5 factors that determine virulence

A
  1. toxins
  2. adhesion factors
  3. evasive factors
  4. invasive factors
  5. mutations (change antigenic profile)
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12
Q

define toxins & toxoids

A
  • poisonous substance released by invaders maybe modified to toxoid for immunization
  • virulence factors removed, but retain antigen for T & B cells given as vaccine
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13
Q

define toxoids endotoxins and exotoxins

A

exo: released during bacterial cell growth
endo: within the cell wall of gram (-) bacteria, small amounts are harmful

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14
Q

describe systematic inflam response syndrome and give aka

A

cytokine storm that happens due to to many infectious agents

  1. potent response causing vasc. collapse and organ failure
  2. sepsis
  3. cytokines destroyed and trigger cascades (kinins and coagulation)
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15
Q

describe adhesion factors & 3 types and examples

A

pathogen’s ability to attach and maybe a site or cell

  1. hemagglutinins-viral glycoproteins that attach to cells in the respiratory tract (flu a/b, measles)
  2. slime- adheres to the host and also protects itself from host’ defenses (pseudomonas, strep on teeth, staph on plastic; urinary cath)
  3. pili fimbriae- hairlike/fringe projections that anchor bacteria to cells (like velcro) (gonorrhea )
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16
Q

define evasive factors and 4 examples

A

evading or avoiding host’s immune sys

  1. coagulase: envelopes invader (staph. aureus)
  2. protease: digests IgA (flu & gonorrhea)
  3. capsules: resist phagocytosis (strep, cryptococcus)
  4. leukocidin: kill by punching holes in membranes of neutrophil and macrophage (staph aureus MRSA)
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17
Q

define invasive factors

A

enzymes that allow penetration of tissues

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18
Q

define change antigenic profile and two types & two examples

A

are mutations in antigen that are antigenic drift (minor) & antigenic shift (major) HIV & FLU

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19
Q

what are the H and N in H1N1 flu virus

A

Hemagglutinins: glycoproteins that attach to cells in resp tract
Neuraminidase: surface enzyme of flu virus allows release of virus’ progeny from infected cells

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20
Q

characteristics of viruses

A
  1. small
  2. obligate must replicate inside cell (has only DNA or RNA (never both))
  3. protein coat (capsid)
  4. some enveloped
  5. may be latent
  6. may be oncogenic
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21
Q

6 steps of virus reprodux

A
  1. adsorption (attachment to target cell membrane)
  2. penetration (enzyme release to weaken CM and allow for penetration)
  3. uncoating (virus’ DNA or RNA takes off protective protein coat to go to nucleus)
  4. replication of genetic material
  5. assembly (assembly of genetic material to make new viruses)
  6. release (budding)
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22
Q

3 ways virus severity varies

A
  1. self-limiting
  2. cell death (herpes)
  3. immune complexes (HBV antigen-antibody complex cause damage)
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23
Q

how do retroviruses funx

A

reverse transcriptase converts RNA–>DNA (HIV)

24
Q

characteristics of bacteria

A
  1. peptidoglycan wall
  2. gram (+) have thick walls that stain purple
  3. gram (-) more layers to wall that stain red
  4. when neither gram (-) or (+) acid fast test used (TB)
  5. can be aerobic or anaerobic
  6. has DNA and RNA
  7. subclass of spirochetes & myobacterium
25
Q

Rickettsiae, Chlamydiae, Ehrlichiae characteristics

A
  1. obligate
  2. rigid cell wall
  3. DNA & RNA
26
Q

coxiella characteristics

A

some vector transmission
contaminated food
inhalation while processing meat

27
Q

fungi characteristics

A

yeasts- waxy
molds- cottony
dimorphic (characteristics of moth yeast and mold)
rigid wall
similar to host (some antifungals toxic because it attack PT cells)
-some only grow in cooler temp

28
Q

give example 3 examples of fungi

A
  1. aspergillosis (aspergilloma fungal ball in lung scar or abscess)
  2. pneumocystis jirovecii : HIV
  3. histoplasmosis: dimorphic infx from bird dropping
29
Q

describe infectious mononucleosis

A
  1. caused by EBV epstein barr virus
  2. 90% infx of population
  3. kissing disease (15-35 y.o.)
30
Q

how does mono attack, signs & symp, diagnosis, complication

A
  1. attacks B lymph (self limiting 2-3 wks)
  2. sore throat, fever, lymphadenopathy, fatigue
  3. presence of Paul Bunnel Davidsohn
    - lymphocytosis (10-20K)
    - positive cold aggluntinin titer
  4. splenomegaly
31
Q

3 dz that have (+) cold agglutinin titer

A

mycoplasm pneumonia
mono
multiple myeloma

32
Q

2 types of UTI and example

A

Upper: kidneys and ureters (pyelonephritis- inflamm of renal parenchymal tissue, systemic sx fever malaise)
lower: bladder urethra (cystitis: inflamm of bladder, sx difficult urination)

33
Q

pathogens associated with UTI

A

gram (-) e coli klebsiella proteus mirabilis

gram (+) positive staph saprophyticus

34
Q

4 ways agents exploit host poor health

A
  1. virulence (adhesion flagella hemolysin)
  2. antibiotic resistance
  3. biofilm formation
  4. colonization
35
Q

4 causes of CAUTI

A

intraluminal
extraluminal
trauma
biofilms

36
Q

What causes organism TB, describe and lab test used, how is it transmitted

A

mycobacterium (rod shaped) outer waxy capsule, aerobic organisms
-acid fast (sent 3 days in a row)
droplet nuclei

37
Q

3 stressor types

A
  1. endogenous- individual is source (physical, emotional)
  2. exogenous- outside source
  3. eustress- positive and growth producing
38
Q

3 stages of General adaptive syndrome

A
  1. alarm
  2. resistance (adaptation) flight or fight
  3. exhaustation (allostatic overload)
39
Q

describe alarm stage and responses

A
  1. stimulate stress response: release catecholamines (Epi, Norepi neuropeptide Y & cortisol (glucocorticoid released from adrenal cortex, causes mobilization of substances & stress response)
  2. brain preps body for axn (alert focused tensed)
    - blood pressure increase, blood shunted to muscles heart and brain
    - GI tract less blood flow can cause sx N/V/D
    - glucose is made available to give energy for muscles and brain
40
Q

describe stage of resistance (adaptation)

A

feeback loop continues until balance in maintained or exhaustation
catecholamine and cortisol will drop when body adapting

41
Q

describe exhaustation/allostatic overload stage

A

resources depleted and wear and tear appear
secretion of neuropeptide Y during chronic stress
-food intake increase, activity decrease, energy stored as fat
-seen in vascular dz :atherosclerosis & vasoconstriction

42
Q

triad of constant stress

A
  1. enlargement of adrenal cortex increase in corticosteriods (mineral corticoid–> aldosterone and glucocorticoid–>cortisol)
  2. atrophy of thymus and other lymphoid structures
    - decreases T cell activity, decrease immunity to infx & cancer
    - increased autoimmune response
  3. bleeding ulcers and inflamm of GI tract
    - decrease blood flow mucosa
    - increase acidity in stomach
    - peristalsis inhibited
43
Q

alarm rxn pathways

A

simultaneous pathways
stress–> ACTH impacts Cortex –> Cortex secretes cortisol–> liver releases glucose
stress –> nerve signal –> medulla –> secretion of Ephinephrine –> increased <3 rate, breathing, blood sugar

44
Q

Hypothalamus Pituitary Adrenal (HPA) Axis

A

stress (stress stimulus may arrive through bloodstream (molecules) or impulse (thoughts) or circadian rhythm–> hypothalamus –> CRH (corticotropin releasing hormone) –>anterior pituitary –>ACTH (adrenocorticotropin hormone) –> Adrenal cortex –> cortisol –> (-) feedback on hypothalamus & anterior pituitary & increased blood glucose, amino acids, fatty acids

45
Q

cortisol rxns

A
  1. gluconeogenesis
  2. catabolism of proteins in muscle, skin, bone, fat tissue
  3. redistribution of fat (lypolysis in extremities & lipogenesis in face & trunk)
  4. immunosuppression
    - Central CRH causes overall weakened immunoresponse to conserve energy
    - Peripheral CRH cause mast cell degranulation (i.e. histamine release)
    - may have more allergic rxns or autoimmune disorders
46
Q

describe ADH & pathway

A

Antidiuretic Hormone
- secreted when blood volume decreases and in response to hypothalamic stimulus (i.e. stress)
hypothalamus –> POSTERIOR pituitary –> release of ADH –> increases blood volume for fight of flight response

47
Q

s/s of metabolic syndrome, aka

A

Syndrome X

  • abdominal obesity
  • abnorm glucose metab
  • increase lipids
  • increase BP
  • 40% of Americans
48
Q

what does hypothalamus affected by, control, monitor, integrate and system is it the master gland of

A
affected by: phys and psych stress
control: h2o balance, temp, body growth & hunger
monitor: feelings of rage passion & fear
integrates: response of SNS & PNS
master gland: endocrine sys
49
Q

in GAS what does coritsol, catecholamines and beta endorphins funx

A

cortisol: increase synthesis of catecholamines
catecholamines: cause insulin resistance and cardiovasc effects
beta endorphins: improves mood, increases social affiliation (oxytoxcin), decrease pain perception, can be depleted

50
Q

5 general aspects of ANS

A
  1. both CNS or PNS, regulated by hypothal. nerve tracts in spinal cord, terminate at effector organs
  2. largely subconcious
  3. regulates adjusts coordinates vital visceral funxs
  4. affects/is affected by emotions
  5. 2 neuron system:
    - ganglion (mass of nervous tissue made up of neuron cell bodies lying outside brain and spinal cord)
    - myelinated neuron connective tissue insulation to speed conduxn
51
Q

Two branches of ANS & perspective neurotransmitters

A

SNS: fight flight noriepi & epi, epinephrine is more potent, & ACH
PNS: rest & digest: ACH

52
Q

Describe when SNS & PNS releases its different neurotransmitters using cholinergic, nicotinic, muscarinic, adrenergic

A

sns pns Preganglionic neurons: release ACH, cholinergic receptors (nicotinic)

PNS postganglionic neurons release ACH, cholinergic receptors (muscarinic)

Most SNS postganglionic neurons release norepi as neurotransmitter, receptors adrenergic (alpha or beta)
-sweat gland postganglionic neurons release ACH, cholinergic receptor (muscarinic)

53
Q

where does nore and epi come from

A

norepinephrine: can be neurotransmitter or come from the medulla
epinephrine: only comes from the medulla

54
Q

1st type of adrenergic receptors & location & response

A

alpha 1: smooth muscle of blood vessels in gut and skin cause vasoconstriction, raises BP shunts blood to lungs liver brain skeletal muscles and <3

alpha 2: located on actual nerves that stimulate effector cells & brain, located on smooth muscle of GI tract: cause relaxn decrease digestion

55
Q

2nd type of adrenergic receptors & location & response

A

beta 1: located on (which increases BP)

Beta 2: located on bronchial smooth muscle: cause bronchodilation, also located on blood vessels in skeletal muscles: cause vasodilation, increases blood flow to muscles