Brainscape's Knowledge GenomeTM

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


See full index

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

describe virchow’s triad

A
  1. hypercoagulability
  2. venous stasis
  3. endothelial damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what causes arterial thrombosis + treatment

A

atherogenesis
* MI
* iscahemic stroke
* PVD

Sx= cold + pale + loss of pulse

Tx= antiplatelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what causes venous thrombosis + Tx

A

venous stasis, DVT

Sx= tender, swollen, red

Tx= anticoagulants (DOACs, warfarin , LMWH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what makes up an atherosclerotic plaque

A
  • lipid
  • smooth muscle
  • macrophages (+foam cells)
  • platelets
  • fibroblasts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

define carcinogenesis
& neoplasm

A

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

neoplasm= autonomous, abnormal, persistent new growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

name benign and malignant epithelial tumours

A

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

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

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

list 5 benign connective tissue tumours

A
  • lipoma- adipocytes
  • rhabdomyoma- striated muscle
  • leiomyoma- smooth muscle cells
  • chondroma- cartilage
  • osteoma- bone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

list 5 malignant connective tissue tumours

A
  • liposarcoma- adipocytes
  • rhabdomyosarcoma- striated muscle
  • leiomyosarcoma- smooth musc. cells
  • chondrosarcoma- cartilage
  • osteosarcoma- bone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

name 4 cells stemming from myeloblasts

which 2 are involved in innate immunity

A
  • eosinophil- parasites
  • basophil (allergy)
  • neutrophil + macrophages = innate immuntiy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

what is the ‘professional antigen presenting cell’ and what does it do

A

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
Q

describe IgG

A
  • most abundant Ig in blood
  • key in 2ndary immune response- marker of immunological memory, v. specific
27
Q

describe IgA

A
  • most abundant Ig in total body
  • found on mucosal linings + in breast milk
  • forms DIMER
28
Q

describe IgM

A

first Ig released in immune response - less specific
forms pentamer

29
Q

describe IgE

A

IgE activates mast cell + basophil degranulation in T1 hypersensitivity

30
Q

describe major histocompatibility complexes and the autoimmune diseases they are asscociated with

A

major histocompatibilty complexes on chromosome 6 aka. HLA molecules

  • HLA B27= spondyloarthropathies
  • HLA DR2/DQ3= T1DM
  • HLA DQ2/8= coeliac
  • HLA B8= SLE
31
Q

describe T1 hypersensitivity reactions

egs

A

IgE mediated
* IgE binds to basophil/mast cell > degranulation > histamine release

egs= asthma, hayfever, rhinitis

32
Q

what are the effects of histamine release

A

vasodialtion + increased permeability (H1 receptor)
bronchoconstriction, facial flushing, pruritis, swollen tongue + face

33
Q

describe T2 hypersensitivity reactions

A

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
Q

describe T3 hypersensitivity reactions

A

immune complex deposition
- IgG/IgA binds to antigen + activates complement @ site of A-A deposition

egs= SLE, post strep glomerulonephritis, IgA glomerulonephritis

35
Q

describe T4 hypersensitivity reactions

A

T cell mediated
TH1 activated by antigen presenting cells- triggers response

egs= DMT1, TB, MS, guillain barre

36
Q

pharm

describe the 2 main routes of administration

+ extras

A

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
Q
A
38
Q

define agonist and anatgonist receptors

define affinity & efficacy

A

agonist= full affinity + full efficacy

antagonists= full affinity + NO efficacy

affinity= how well it binds
efficacy= how well receptor is activated

39
Q

define drug strenght + potency

A

how much drug is needed to ellicit response in the body= potency

40
Q

define Emax and EC50

A

Emax= maximal value (efficacy)
EC50= value of 50% of sigmoid (halve maximal response)

41
Q

describe anatgonist mechansim

A

antagonists= competitivley (compete for active site) or non-competitivley (allosteric) INHIBIT receptors

42
Q

describe the mechansims of the diuretics:
1. loop
2. thiazides
3. spironolactone

A
  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
Q

what is the action of calcium channel blockers

egs

A

CBB= amlodipine, verapamil,dilitazem
> Ca influx= vasoconstriction + increased contractability

44
Q

describe the action of lidocaine

A

local anaesthesia
-blocks Na+ voltage gated channels therefore no Na influx therefore no action potentials

45
Q

define pharmacokinetics and pharmacodynamics

A

pharmacokinetics =what the body does to the drug
pharmacodynamics= what the drug does to the body.

46
Q

what happens to a drug in body = ADME

describe drug administration

define bioavailiability

A

administration= route + entry into body

bioavailiability= how fast and to what extent the drugs reaches systemic circualtion
IV= always 100%

47
Q
A
48
Q

ADME

describe distribution

A

drug distributed in plasma according to chemical properties + size
-may be uptaken by some organs eg liver, brain

49
Q

ADME

describe drug metabolism

describe rate + phase

A

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
Q
A
51
Q

ADME

describe drug excretion

A

in urine + faeces- mostly by kidneys

52
Q
A

Phase 2a (12 decks)

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