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Phase 2a > ICS + PATH + IMM + PHARM > Flashcards

ICS + PATH + IMM + PHARM Flashcards

1
Q

what cells are associated with a. acute and b. chronic inflammation

A

acute inflammation (infections, hypersensitivity)= neutrophils

chronic inflammation (autoimmunity, recurrent infections) = macrophages, lymphocytes

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2
Q

list the 5 cardinal signs of inflammation

A
  1. rubor (red)
  2. dolor (pain)
  3. calor (heat)
  4. tumour (swelling)
  5. loss of function
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3
Q

describe the 3 stages of inflammation

A
  1. vasodilation (inflammatory cytokines- bradykinin, prostaglandin)
  2. fluid exudate - vessel becomes leaky
  3. neutrophils become abundant in exudate
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4
Q

describe neutrophil action in acute inflammation

A

margination (move 2 edge)
adhesion
emigration + diapedesis (movement out of blood vessel)
chemotaxis _ move to site of inflammation

@ the site

phagocytosis > phagosomal + bacterial killing > macrophages clear debris

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5
Q

what are the 4 outcomes of acute inflammation

A
  1. resolution (norm)
  2. supporation (pus)
  3. organisation (granulation tissue + fibrosis)
  4. progression (chronic fibrotic tissue)
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6
Q

granulomatous diseases

what do granulomas secret

A

sarcoidosis
leprosy (SLE)
vasculitis
crohn’s

TB= caseating granulomatous disease

granulomas secrete ACE - blood marker increased in those w. granulomatous diseases

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7
Q

describe virchow’s triad

A
  1. hypercoagulability
  2. venous stasis
  3. endothelial damage
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8
Q

what causes arterial thrombosis + treatment

A

atherogenesis
* MI
* iscahemic stroke
* PVD

Sx= cold + pale + loss of pulse

Tx= antiplatelets

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9
Q

what causes venous thrombosis + Tx

A

venous stasis, DVT

Sx= tender, swollen, red

Tx= anticoagulants (DOACs, warfarin , LMWH)

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10
Q

what makes up an atherosclerotic plaque

A
  • lipid
  • smooth muscle
  • macrophages (+foam cells)
  • platelets
  • fibroblasts
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11
Q

describe the formation of an atherosclerotic plaque

A
  1. fatty streak= precursor to plaque (over 10yrs +)
  2. lipid accumulation- increased LDL, macrophages phagocytose these to FOAM CELLS
  3. platelet aggregation- plaque protudes into artery lumen> disrupts laminar flow- therefore platelet accumulation + thinning of media
  4. fibrin mesh + RBC trapping- platelt plug form smesh over itself (secondary stable clot) rbcs trapped within this
  5. fibrous cap- fibroblasts form smooth musc. cap over 2ndary platelet plug= stable atheroma

unstable atheroma (angina- ACS)> fibrous cap damaged + continous platelet plug formation over this = narrowed

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12
Q

define:
* metaplasia
* dysplasia

A

metaplasia= change of one cell type into another cell type (barrett’s oesophagus)

dysplasia= change of differentiated cell type into poorly differentiated type (mostly pre cancerous)

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13
Q

define carcinogenesis
& neoplasm

A

carcinogenesis= transforamtion of normal cells into neoplastic cells via permanent mutation

neoplasm= autonomous, abnormal, persistent new growth

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14
Q

name benign and malignant epithelial tumours

A

benign=
-papilloma (nonglandular tissue)
-adenoma (secretory tissue)

malignant=
-carcinoma (epithelial cells)
-adenocarcinoma (glandular epithelium)

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15
Q

list 5 benign connective tissue tumours

A
  • lipoma- adipocytes
  • rhabdomyoma- striated muscle
  • leiomyoma- smooth muscle cells
  • chondroma- cartilage
  • osteoma- bone
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16
Q

list 5 malignant connective tissue tumours

A
  • liposarcoma- adipocytes
  • rhabdomyosarcoma- striated muscle
  • leiomyosarcoma- smooth musc. cells
  • chondrosarcoma- cartilage
  • osteosarcoma- bone
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17
Q

name 5 classes of carinogens and give some examples

A
  1. chemical eg paint, dye, rubber
  2. viruses eg EBV (burkitts), HPV (cervical cancer)
  3. ionising + non-ionising radiation- UVB in skin cancer
  4. hormones, parasites, mycotoxins eg increased oestrogen
  5. asbestos
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18
Q

list 3 methods of mestastatic spread

what are the five main mets to bone

A
  1. haematogenous- via blood
  2. lymphatic= secondary formation in lymph nodes eg lymphoma
  3. transcolemic= via exudative fluid accumulation, spread via plueral, pericardial + peritoneal effusions

kidney (renal cel)
prostate

BLT KP
breast
lungs
thyroid

sarcomas= mostly haemotgenous
carcinomas= mostly lymphatic (exceptions = follicular thyroid, RCC, HCC)

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19
Q

which cancers are screened for in the uk and test is used in each

A
  • cervical- cervical swab
  • breast- mammogram
  • colorectal- fecal occult
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20
Q

name 4 cells stemming from myeloblasts

which 2 are involved in innate immunity

A
  • eosinophil- parasites
  • basophil (allergy)
  • neutrophil + macrophages = innate immuntiy
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21
Q

name 4 cells stemming from common lymphoid progenitor cells

A

adaptive immunity=
* natural killer cells
* T cell
* B cell > differentiates 2 plasma cell

22
Q

name 5 barriers in innate immunity

A

physcial= skin, mucus, cilia
chemical= lysozymes in tears, stomach acid

23
Q

how does the compliment system destroy forgein antigens

A
  • direct lysis- membrane attack complex formation
  • opsonisation- increased phagocytosis
  • inflammation- macrophage chemotaxis
24
Q

what kind of receptors are in haemopoetic cells and what do they respond to

A

TOLL like receptors (TLR)+ nod like receptors
- respond to pathogen associated molecular patterns
- damage associated molecular patterns

lectins in blood bind pathogen after TLRs activated

this triggers immune response- activate complement, stimulate cytokine release

25
what is the 'professional antigen presenting cell' and what does it do
dendritic cell- present forgein antigens to Th cell =stimulates further TH proliferation + B cell prodution > antibodies | macrophage, b cell can also be apc but dendritic= best
26
describe IgG
* most abundant Ig in blood * key in 2ndary immune response- marker of immunological memory, v. specific
27
describe IgA
* most abundant Ig in total body * found on mucosal linings + in breast milk * forms DIMER
28
describe IgM
first Ig released in immune response - less specific forms pentamer
29
describe IgE
IgE activates mast cell + basophil degranulation in T1 hypersensitivity
30
describe major histocompatibility complexes and the autoimmune diseases they are asscociated with
major histocompatibilty complexes on chromosome 6 aka. HLA molecules * HLA B27= spondyloarthropathies * HLA DR2/DQ3= T1DM * HLA DQ2/8= coeliac * HLA B8= SLE
31
describe T1 hypersensitivity reactions | egs
**IgE mediated** * IgE binds to basophil/mast cell > degranulation > histamine release | egs= asthma, hayfever, rhinitis
32
what are the effects of histamine release
vasodialtion + increased permeability (H1 receptor) bronchoconstriction, facial flushing, pruritis, swollen tongue + face
33
describe T2 hypersensitivity reactions
**antigen-antibody complex** IgG/M bonds to antigen + activates MAC (complement) @ site of A-A binding | egs= good pasture's, pernicious anaemia, rheumatic fever
34
describe T3 hypersensitivity reactions
**immune complex deposition** - IgG/IgA binds to antigen + activates complement @ site of A-A deposition | egs= SLE, post strep glomerulonephritis, IgA glomerulonephritis
35
describe T4 hypersensitivity reactions
**T cell mediated** TH1 activated by antigen presenting cells- triggers response | egs= DMT1, TB, MS, guillain barre
36
# pharm describe the 2 main routes of administration | + extras
enteral= GIT involved eg oral (PO) parenteral= non-GIT: IM, IV, SC injection w local or systemic affects | also= inhaled- ICS topical- cream rectal- suppository
37
38
define agonist and anatgonist receptors | define affinity & efficacy
agonist= full affinity + full efficacy antagonists= full affinity + NO efficacy | affinity= how well it binds efficacy= how well receptor is activated
39
define drug strenght + potency
how much drug is needed to ellicit response in the body= potency
40
define Emax and EC50
Emax= maximal value (efficacy) EC50= value of 50% of sigmoid (halve maximal response)
41
describe anatgonist mechansim
antagonists= competitivley (compete for active site) or non-competitivley (allosteric) **INHIBIT** receptors
42
describe the mechansims of the diuretics: 1. loop 2. thiazides 3. spironolactone
1. loop (furosemide)= inhibits NKCC2 symporter in ascending limb 2. thiazides (bendroflumethiazide)= inhibitors Na-Cl co-transporter in DCT 3. spironolactone= K+ sparing diuretic- aldosterone inhibitor
43
what is the action of calcium channel blockers | egs
CBB= amlodipine, verapamil,dilitazem > Ca influx= vasoconstriction + increased contractability
44
describe the action of lidocaine
local anaesthesia -blocks Na+ voltage gated channels therefore no Na influx therefore no action potentials
45
define pharmacokinetics and pharmacodynamics
**pharmacokinetics** =what the body does to the drug **pharmacodynamics**= what the drug does to the body.
46
# what happens to a drug in body = ADME describe drug administration | define bioavailiability
administration= route + entry into body **bioavailiability= how fast and to what extent the drugs reaches systemic circualtion** IV= always 100%
47
48
# ADME describe distribution
drug distributed in plasma according to chemical properties + size -may be uptaken by some organs eg liver, brain
49
# ADME describe drug metabolism | describe rate + phase
drugs metabolised in kidney or liver: kidney= mostly small water soluble liver= hydrophobic molecules metabolism classified by rate (first order, second order etc) and phase
50
51
# ADME describe drug excretion
in urine + faeces- mostly by kidneys
52

Phase 2a (12 decks)

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