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POM > week 3 > Flashcards

week 3 Flashcards

1
Q

what body temperature is considered a fever?

A

100.4 F, 38.5 C

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2
Q

____ days and under, a child must undergo a full sepsis workup (labs, XR, cultures, LP) for every fever

A

28

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3
Q

phases of wound healing:

A

inflammatory (includes extravasation)
proliferative (granulation)
remodeling (maturation)

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4
Q

what are the stages of the inflammatory phase of wound healing?

A

hemostasis

  • platelet aggregation
  • vasoconstriction for a short time

clotting

  • fibrinogen turned to fibrin (via thrombin)
  • clotting factors (collagen and basement membrane proteins)

vasodilation

  • histamine and nitric oxide release
  • extravasation - migration of leukocytes, edema, toxic debris dilution etc.
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5
Q

what are the phases of extravasation? list the proteins/receptors associated with each.

A

rolling

  • selectin on endothelium
  • sialyl Lewis X on leukocyte
  • allows the leukocyte to “roll” across the endothelium

adhesion

  • ICAM, VCAM on endothelium
  • integrin on leukocyte (activated by cytokines from macrophage)
  • binds/adheres strongly to the endothelium

transmigration/diapedesis

  • PECAM on both endo and leuk
  • leukocyte passes through the endothelium

migration
-leukocyte migrates and binds to the ECM of the wound site (using integrin)

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6
Q

what occurs during the proliferative phase?

A 
fibroblasts migrate in 
-collagen III
-collagen I
granulation (primary tissue to form)
angiogenesis 
epithelialization
wound contraction
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7
Q

describe the remodeling phase?

A

reorganization of the collagen composition
collagen crosslinking
tissue becomes more normal/stable

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8
Q

types of scars:

A

keloid: overgrowth of collagen, past the wound’s boundaries
hypertrophic: raised, red, and itchy; does not extend past boundary
atrophic: indented, e.g. acne scars

stretch marks

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9
Q

list the 3 types of intention:

A

primary - clean cut surgical incision, no infection
secondary- due to injury or trauma, ragged edges, can be infected, results in scaring
tertiary or delayed primary - left open due to possibility of infection, grafts, a lot of scarring

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10
Q

effects of competitive inhibition:

A

Km increase
-need more substrate in order to outcompete the inhibitor and to bind half the enzyme’s active sites

Vmax same
-if it outcompetes, it has the potential to have the same end result

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11
Q

describe the role of malate in inhibtion:

A

malate is a competitive inhibitor in fumarate synthesis
binds to the enzyme complex that typically binds succinate (substrate analogue, same 3D shape)

succinate + enzyme —-> fumarate and enzyme

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12
Q

describe the relationship between Km and enzyme affinity

A

increasing Km, lowering affinity (need more substrate for same job)
decreasing Km, increasing affinity (can do the same job for a lot less)

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13
Q

what drugs inhibit folic acid synthesis from PABA + pteridine and glutamic acid?

A

sulfa drugs

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14
Q

issues with methanol metabolism:

A

forms formic acid which causes metabolic acidosis, neurotoxicity, and causes direct damage to the optic nerve (visual impairments or blindness)

treatment for methanol poisoning: treat patient with ethanol/fomepizole (alcohol DH competitive inhibitor, blocks the formation of formaldehyde and therefore formic acid)

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15
Q

issues with ethylene glycol metabolism:

A

produces oxalic acid (toxic)
forms with calcium to form calcium oxalate in the kidneys: renal necrosis (nephrotoxic)

treatment: treat patients with ethanol/fomepizole (alcohol dehydrogenase) competitive inhibitor, prevents the formation of glycol aldehyde

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16
Q

target enzyme and therapuetic use: STATINS

A

HMG-CoA reductase

decrease plasma cholesterol, anti-hyperlipidemic drug

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17
Q

target enzyme and therapeutic use: allopurinol

A

xanthide oxidase, gout

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18
Q

target enzyme, therapeutic use: methotrexate

A

dihydrofolate reductase, cancer

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19
Q

target enzyme, therapeutic use: captopril, enalpril

A

angiotensin converting enzyme: HTN

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20
Q

target enzyme, therapeutic use: dicoumarol

A

vitamin K epoxide reductase, anticoagulant

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21
Q

effects of noncompetitive inhibitor:

A

Km no change

Vmax decreased

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22
Q

effects of Uncompetitive inhibition?

A

Kmax decrease

Vmax decrease

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23
Q

alanine and ATP are _____ inhibitors of _______.

A

noncompetitive, pyruvate kinase

explanation: pyruvate breaks down into alanine and an ATP molecule is generated when pyruvate is produced, when these products build up it signals to the glycolic pathway that it should slow down. prevents energy wasting.

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24
Q

cyanide is a __________ inhibitor of ____________.

A

irreversible, cytochrome C oxidase (ETC)

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25
Q

___________(drug) inhibits the activity of __________(enzyme) in treatment for AIDS.

A

NNRITs, reverse transcriptase

NNRIT (no nucleoside reverse transcriptase inhibitor) blocks the conversion of HIV RNA into HIV DNA (via blocking reverse transcriptase)

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26
Q

effects of prostacyclin (PGI2):

A
  • produced mostly in epithelium
  • INHIBITS platelet aggregation (increases cAMP)
  • vasodilation

**opposing effect of thromboxane A2

**injury to the vessel wall inhibits its synthesis so that platelet aggregation can occur

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27
Q

effects of thromboxane A2:

A
  • produced mainly in the platelets
  • PROMOTES platelet aggregation (decreases cAMP)
  • vasoconstriction
  • mobilize cellular calcium
  • contraction of smooth muscle

**opposing effect of prostacyclin (PGI2)

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28
Q

effects of prostaglandin E2:

A
  • VASODILATION
  • relaxes smooth muscles
  • modulation of inflammation
  • causes FEVER and PAIN
  • used to induce labor

**role in inflammation by increasing capillary permeability, erythema and wheel formation

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29
Q

effects of prostaglandin F2alpha:

A
  • VASOCONSTRICTION
  • contracts smooth muscles
  • stimulates uterine contractions
  • role in LH induced ovulation
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30
Q

what drug inhibits phospholipase A2?

A

corticosteroids (e.g. annexin A1)

**phospholipase A2 releases AA from the phospholipid membrane in response to a stimulus

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31
Q

what drug inhibits COX 1 and COX2?

A

COX1: low dose Aspirin, NSAIDS

COX2: Aspirin (higher dose?), NSAIDs, Coxibs

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32
Q

how does aspirin inhibit COX1?

A
  • acetylates the serine OH reside in the enzymes channel
  • IRREVERSIBLE inhibition
  • this bulky addition prevents AA from accessing the channel
  • thromboxane production is prevented
  • therefore, platelet aggregation decreases (anti-thrombotic property of ASA)
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33
Q

what is the optimum temperature for enzyme activity/metabolism in humans?

A

37 deg C

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34
Q

posterior hypothalamus responds to cold sensed by skin thermoreceptors by:

A

skeletal muscles

  • increases shivering
  • ATP to ADP (exothermic)

sympathetic NS - catecholamines (epi, nepi)

  • alpha 1 receptors in blood vessels/ vascular smooth muscle: vasoconstriction (reduced heat loss)
  • B receptors in brown adipose tissue: burns calories to generate heat
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35
Q

anterior hypothalamus responds to increasing temperatures by:

A

stimulating sympathetic cholinergic receptors: stimulate sweat glands to increase sweating (evaporative cooling)

decreases sympathetic activity in vasculature/blood vessels - vasodilation, increase blood flow to skin, increase heat loss

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36
Q

what are the phases of heat stress?

A
  1. heat cramps
  2. heat syncope - lack of adequate blood to the brain
  3. heat exhaustion - acute plasma loss
  4. heat stroke - hypothalamus failing, dry hot skin
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37
Q

what is the process for heat adaptation to warm climates?

A

2 week process
increase sweating rate, sweat earlier
decreased salt excretion in urine
more salt reabsorbed via aldosterone – increased water retention

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38
Q

what is the feedforward process between the skin thermoreceptors and hypothalamus?

A

the skin senses a change in the environmental temperature and signals to the hypothalamus before the core body temperature drops or raises

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39
Q

what is the normal body skin temperature?

A

31-36 C (91 F)

40
Q

describe the phases of fever:

A
  • pyrogens stimulate interleukin-1 to be released by phagocytes (e.g. neutrophils)
  • interleukin 1 stimulates local prostaglandin production (PGE2 especially)
  • signals to the anterior hypothalamus that the set point needs to be higher, makes core body temperature appear “too low”
  • body attempts to increase temperature through chills, piloerection, epinephrine, shivering)
  • body reaches the set temperature and the fever “breaks” - sweating, vasodilation
  • body temperature decreases to normal and set point goes back down to normal
41
Q

what is the epimysium and what is its function?

A

the outermost sheath surrounding muscle

function: protects the muscle from friction against other muscles and bones, maintains the structural integrity, separates the muscle from other tissues/organs in the area

42
Q

what is the perimysium and what is its function?

A

each perimysium surrounds a fascicle (bundle) of muscle fibers, allows the nervous system to innervate specific muscle groups, eliciting specific movements

compartmentalization determines the movement a muscle will make

43
Q

what is the endomysium and what is its function?

A

thin connective tissue that surrounds the individual muscle fiber (myocyte), contains extracellular fluids and nutrients to support the muscle fiber (supplied via blood), allows the muscle fibers to glide past one another to an extent

44
Q

what metaplastic changes are associated with the lower esophagus?

A

stratified squamous (non keratinized) epithelium of the lower esophagus is replaced by simple columnar of the stomach

“Barret Mucosa”

causes: GERD, alcohol, smoking

45
Q

what metaplastic changes are associated with the secondary bronchi?

A

pseudostratified ciliated columnar epithelium are replaced by stratified squamous non keratinized epithelium

cause: smoking

46
Q

explain the dysplastic process of the uterine cerivx:

A

stratified squamous non keratinized epithelium are replaced by a rapid growth of cells without differentiation

normally, stem cells above basement membrane with stratified squamous at the top. in abnormal histology image, abnormal cells take up the whole length. no differentiation between stem cells and stratified squamous. also, there is a large nucleus:cytoplasm ratio.

**dysplasia also commonly affects the skin

47
Q

what is anaplasia?

A

tumor does not resemble the parent tissue

48
Q

what is pleomorphism?

A

variation in the size and shape of cells of a tissue

-range from small undifferentiated tissue to tumor giant cells

49
Q

what is the morphology of abnormal cancer cells?

A

abnormal 1:1 nucleus to cytoplasm ratio (usually 1:4, 1:6)
abnormal shape
hyperchromatic nucleus

loss of polarity - sheets and large masses of tumor cells grow in a disorganized fashion
mitotic cells are distributed throughout the thickness of the epithelium

50
Q

pre-invasive neoplasm vs. invasive neoplasm

A

a pre-invasive neoplasm is carcinoma in situ (the dysplasia involves full thickness of the epithelium but it does not invade the basement membrane)

an invasive neoplasm is a dysplasia that involves full thickness and it also invades the basement membrane

51
Q

what are kaliocytes?

A

“halo cells” - looks like a larger nucleus with a halo of cytoplasm around it

type of epithelial cell that develops following an HPV infection

52
Q

what are the stages of cervical intraepithelial neoplasia (CIN)?

A

CIN 1 - 1/3 abnormal
CIN 2 - 2/3 abnormal
CIN 3 - full thickness of the epithelium

53
Q

what are the stages of breast cancer?

A

o - abnormal cells are present but have net yet spread
I - early stage (spread to tissue in a small area)
II - localized (20-50 mm with some lymph node involvement)
III - regional spread (larger than 50 mm, larger lymph involvement)
IV - distant spread (spread beyond breast and to other regions of the body)

54
Q

some bacteria are coated in a ______capsule that prevents __________.

A

polysaccharide, phagocytosis

55
Q

describe the gram staining process:

A

1) crystal violet
2) fixed with iodine
3) washed with ethyl alcohol (decolorization)
4) Safranin counterstain

56
Q

what is an acid fast stain?

A

AKA Ziehl Neelsen stain
acid fast = high mycolic acid - stains pink
non-acid fast stain blue

e.h. mycobacterium (Tb) is an acid fast

57
Q

endospore stain:

A

AKA Schaffer Fulton Stain
malachite green binds spores
pink bacteria

58
Q

what’s a mesophile?

A

need medium temperature (37 C) for optimum growth

59
Q

what is a neutrophile?

A

need neutral pH (6.5-7) for optimum growth

60
Q

what is a microaerophile?

A

requires oxygen but at LOW concentrations

61
Q

major differences between endotoxins and exotoxins:

A

endotoxins:

  • part of LPS cell wall of gram -
  • heat stable
  • no vaccines
  • not as antigenic
  • pyrogen
  • released through cell lysis

exotoxins:

  • gram + or -
  • heat labile
  • vaccines available
  • high toxicity/highly antigenic
  • may be a pyrogen
62
Q

explain the process of gram (-) sepsis (endotoxemia)

A

endotoxins stimulate the coagulation cascade (fibrin is deposited at the infection site)

endotoxins stimulate macrophages and monocytes –> release TNF and Interleukin-1 —> cascade of secondary messengers (i.e. prostaglandins, interferons, platelet activating factors)

leads to shock, multi-organ dysfunction (MODS). excessive activation of the coagulation cascade can lead to disseminated intravascular coagulation (DIC)

**endotoxins can also stimulate the alternate complement cascade

63
Q

why is treating endotoxins with Abx bad?

A

since endotoxins are a part of the gram negative membrane, the Abx would cause bacterial lysis and would release the endotoxins

64
Q

streptococcus pyogenes:

A

gram (+) bacteria, exotoxins, “group A strep”, arranged in chains

can cause scarlet fever and strep throat

65
Q

features of scarlet fever:

A
  • pyrogenic (fever)
  • erythematous rash
  • pharyngitis
  • white coated tongue followed by a strawberry tongue
66
Q

streptococcal TSS:

A 
streptococcus pyogenes 
streptococcal super antigens (StrepSAgs)
invasive group A strep infection
leads to shock, organ failure, hypotension, tachycardia 
fever is common, AMS in half of cases 
influenza like syndrome in 20%
67
Q

staphylococcal TSS:

A 
gram (+), staph aureus 
arranged in CLUSTERS 
rapid onset of fever, rash, hypotension, multi organ system involvement
menstrual associated cases 
staphylococcal superantigens (staphSAgs)
68
Q

what are defensins?

A

cationic proteins found in vertebrates, invertebrates, and plants

active against bacteria, viruses, and enveloped viruses

69
Q

what are defensins?

A

cationic proteins found in vertebrates, invertebrates, and plants

active against bacteria, fungi, and enveloped viruses

70
Q

what are cathelicidins?

A

small antimicrobial peptides that induce holes in bacterial membranes

also active against bacteria, fungi, and enveloped viruses

71
Q

what pathogens have terminal mannose residues?

A

bacteria and fungi

this is a PAMP

72
Q

what pathogen has unmethylated CG rich oligonucleotides (CPG)?

A

microbials

this is a PAMP

73
Q

which TLR target extracellular PAMPS?

A

1, 2, 4, 5, 6 (skip 3)

“E comes before I”

74
Q

which TLRs target intracellular PAMPS?

A

3, 7, 8, 9

75
Q

what is the result of activating TLRs?

A

releases cytokines and adhesion molecules, activates phagocytes and other cells

76
Q

what is the role of NOD-like receptors?

A

inflammation, target gene expression of inflammatory proteins

77
Q

what PAMPS do NOD like receptors detect?

A

“north carolina”

cytosolic pathogens

78
Q

what PAMPs do RIG like receptors respond to?

A

viral “R”NA in the cytosol

induce inflammation and antiviral type 1 interferons (e.g. interferon alpha)

79
Q

what PAMPs do cytosolic DNA sensors respond to?

A

microbial dsDNA in the cytosol
increase the production of type 1 interferons
induces autophagy

80
Q

what two types of Pattern Recognition Receptors (PRRs) release type 1 interferons (IFNs) when they find their PAMP?

A

RIG like (viral RNA) and Cytosolic DNA sensors (CDs)

81
Q

what types of cells are involved in the innate immune response?

A 
neutrophils
macrophages 
eosinophils, mast cells, basophils
dendritic cells
innate lymphoid cells 
natural killer cells (NK cells)
82
Q

what kills microbes inside the lysosome?

A

oxidase - RoS
inducible nitric oxide synthetase (iNOS)
lysosomal proteases

83
Q

what are the pro-inflammatory cytokines?

A

IL-1, IL-6, IL-12, IL-18, TNF alpha, IFN gamma (interferon gamma), GM-CSF (granulocyte-macrophage colony stimulating factor)`

84
Q

what are the 2 outcomes of the innate immune response?

A

acute inflammation and antiviral defense

acute inflammation: involves accumulation and activation of leukocytes and plasma proteins at the site of injury, increased permeability of the blood vessels, increased expression of adhesion molecules

antiviral defense: virally infected cells and specialized dendritic cells (plasmacytoid DC) secrete Type 1 interferons: IFN alpha and beta, work in a paracrine fashion to set up an antiviral response in adjacent cells

(IF YOU SEE VIRAL OR MICROBIAL dsDNA, THINK INTERFERONS. IFN INTERFERES WITH VIRAL REPLICATION)

85
Q

what are the 2 clinical markers of inflammation?

A

1) C reactive protein: increases with increasing pro-inflammatory cytokines (IL-1, IL-6, TNF alpha); directly proportional to inflammatory intensity
2) erythrocyte sedimentation rate (ESR): rate at which erythrocytes settle in plasma, fibrin enters blood in high amounts during inflammation. so more RBCs clumping = higher ESR)

86
Q

what are the stages of complement action?

A

pattern recognition trigger
proteolytic cleavage cascade

leads to inflammation, phagocytosis, membrane attack (MAC complex)

87
Q

what are the pattern recognition triggers for each of the 3 complement pathyways?

A

classical: IgG and IgM
alternative: a specific antigen
lectin: mannose

88
Q

what are the functions of the complement?

A

opsonization
cell lysis
inflammation/recruitment
stimulate B cell response/antibody recruitment

89
Q

what is the individual function of the C3b protein

A

opsonization

recognized by phagocytic receptors

90
Q

what is the function of the MAC complex?

A

penetrates membranes
osmotic lysis
targets thin membranes (i.e. gram neg bacteria)

91
Q

what is the individual role of C3a and C5a?

A

chemotaxins/anaphylatoxins
induce inflammation
chemo-attract other neutrophils, eosinophils, monocytes, macrophages
anaphylatoxins-release inflammatory molecules by mast cells, phagocytic cells, and endothelial cells; causes smooth muscle contraction, bronchial constriction, increased vascular perm.

92
Q

what is the role of C3d of the alternative pathway?

A

recognized by receptor on B lymphocytes
increases B cell response
example of where the innate response (complement) activates the adaptive (B cells, antibodies)

93
Q

what are the regulatory proteins that keep the complement pathway turned off in the absence of pathogen?

A

C1 inhibitor (C1 INH)
Decay Accelerating Factor (DAF)
Factor I and Factor H

94
Q

C1 inhibitor…

A

complement pathway
stops early, at C1 activation stage
prevents it from gaining proteolytic activity

95
Q

Decay Accelerating Factor (DAF)

A

disrupts the binding of Bb to C3b (alternative)
also disrupts the binding of C4b to C2a (classical, lectin)
prevents C3 convertase formation

96
Q

Factor H and I

A

plasma proteins that cleave C3b into inactive fragment iC3b, cannot propagate the alternative pathway

POM (6 decks)

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