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Haroons notes Flashcards

1
Q

What is inflammation?

A

Acute/chronic tissue injury response

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2
Q

What is the difference between acute and chronic inflammation?

A

Acute - infections, hypersensitivity (neutrophils)
Chronic - think autoimmunity, recurrent infections (macrophages, lymphocytes)

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3
Q

What are neutrophils like?

A

‘Polymorphs’ - have many lobes (varying number)
May see Barr bodies in female neutrophils (visible silenced X chromosome - lyonisation)

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4
Q

What are the 5 cardinal signs of inflammation?

A

Rubor, dolor, calor, tumor, loss of function

Redness, pain, heat, swelling

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5
Q

What are the stages of inflammation?m

A
  1. Increased vessel calibre - inflamm. cytokines - bradykinin, prostacyclin, NO. Mediate vasodilation
  2. Fluid exudate - vessel becomes leaky - fluid is forced out of vessel
  3. Cellular exudate - neutrophils become abundant in this exudate
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6
Q

What is neutrophils action in acute inflammation?

A

Margination - migrate to edge of BV
Adhesion - (selectins bind neutrophil, cause rolling along BV margin)
Emigration + diapedesis (movement out of BV - through or in between endothelium)
Chemotaxis -> site of inflammation

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7
Q

What occurs at the site of inflammation?

A

(Neutrophil action)
1. Phagocytosis
2. Phagolysosome + bacterial killing
3. Macrophages clear debris

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8
Q

What are the outcomes of acute inflammation?

A

Resolution (normal)
Supporation (purforration)
Organisation (granulation tissue + fibrosis) (cardiac tissue + neurons never resolve; most become this)
Progression (excessive recurrent inflammation -> becomes chronic + fibrotic tissue)

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9
Q

What are granulomas?

A

Aggregates of epitheloid histology (essentially macrophages)
From granulomatous ‘horseshoe’ shape
Central necrosis () -> classically TB
No central necrosis -> sacrolosis, leprosy, vasculitis (GCA,GPA,EGPA), crohns

Granuloma + eosinophil + parasite
Granulomas secrete ACE -> blood marker (increase in Pxw, granulomatous disease)

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10
Q

What are thrombi + emboli?

A

Thrombosis -> mass of blood constituents (mostly platelets) forming in vessels

  1. Vasospasm
  2. Primary platelet plug - vWF binds to exposed collagen and platelets bind to this (gp1b - activation -> discoid -> pseudopoid) - watch other - gp2a/3b - aggregation
  3. Coagulation cascade
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11
Q

What influences thrombosis?

A

Virchows triad

Endothelial injury
Decrease in blood flow
Hypercoagulability

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12
Q

What are the types of thrombosis?

A

Arterial- atherogenesis - other conditions etc

Venous - venous stasis - etc

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13
Q

What are the fates of thrombi?

A

Resolution - degrades, normal
Organisation - leaves scar tissue behind
Embolism - fragments of thrombi break off + log in distal circulation

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14
Q

What are emboli?

A

Thrombi fragments
Can be:
- arterial - lodges in systemic circulation (from left heart)
- venous - lodges in pulmonary circulation (from right heart)

Further conditions etc

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15
Q

What is atherosclerosis?

A

Plaques forming in intima + media of high pressure vessels (arteries)

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16
Q

What’s in a plaque?

A

Lipid, smooth muscle, macrophages (+foam cells) platelets, fibroblasts

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17
Q

What are foam cells?

A

Macrophages that phagocyte LDLs

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18
Q

What is the formation of atherosclerosis?

A
  1. Fatty streak - precursor to plaque ~ 10 years old
  2. Lipid accumulation - increase in LDL, macrophages recruited to phagocyte this; foam cells
  3. Platelet aggregation - plaque protrudes into artery lumen, disrupts laminar flow, so platelets accumulate here. Thinning of media occurs
  4. Fibrin mesh + RBC trapping - platelet plug forms fibrin mesh over itself (stable 2 clot) + RBCs trapped within this
  5. Fibrous cap - fibroblasts form smooth muscle cap over the 2 platelet plug -> this is a stable atheroma
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19
Q

What occurs in unstable Atheromas?

A

-> in unstable atheromas (angina -> ACS); fibrous cap damaged + continuous platelet plug formation over this, lumen narrowed

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20
Q

What occurs in unstable Atheromas?

A

-> in unstable atheromas (angina -> ACS); fibrous cap damaged + continuous platelet plug formation over this, lumen narrowed

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21
Q

What are risk factors for atherosclerosis?

A

DM, hypertension, smoking, obesity, increased age, male (all RF for MI!)

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22
Q

What is apoptosis?

A

Non-inflammatory controlled cell death
Cell shrink organelles retained + csm intact. Chromatin unaltered; fragmented for easy phagocytosis.

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23
Q

What are the mechanisms for apoptosis?

A
  1. Intrinsic
    - Bax (protein inhibited by Bcl2) acts on mitochondrial membrane to promote cytochrome C release
    - activates caspases -> apoptosis
  2. Extrinsic
    - Fas-L or TNF-L binds to csm receptors which activate caspases -> apoptosis
  3. Cytotoxic
    - CD8+ binding releases granzyme B from CD8+ cell; granzyme B -> perforin -> caspases -> apoptosis
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24
Q

What is necrosis?

A

Inflammatory traumatic cell death
- cells burst, organelles splurge, csm damaged, chromatin altered - cell is fd

Coagulation (mc, due to organ ischaemia), liquefaction (brain becomes soup), caseous (TB; soft cheese!), gangrene (black due to deposited FeS from Hb)

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25
Q

Define hypertrophy

A

Cell gets bigger

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26
Q

Define hyperplasia

A

Number of cells increase in mitosis

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27
Q

Define atrophy

A

Number or size of cell decreases

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28
Q

Define metaplasia

A

Change of one cell type to another type
E.g. Barrett’s oesophagus

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29
Q

Define dysplasia

A

Change of a differentiated cell type -> poorly differentiated type - mostly indicates pre/cancerous change

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30
Q

Define ischemia

A

Decreased perfusion to tissue without infarction e.g. TIA

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31
Q

Define infarction

A

Decreased perfusion with infarction e.g. ischemic stroke

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32
Q

What is carcinogenesis?

A

Transformation of normal -> neoplastic cells through permanent mutation

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33
Q

What is neoplasm?

A

Neoplasm = autonomous, abnormal, persistent new growth
Can only arise from nucleated cells -> can’t arise from erythrocytes but can from their precursors!

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34
Q

What is a tumour?

A

Any abnormal swelling
Neoplasm + inflammation, hypertrophy, hyperplasia all included!

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35
Q

What are tumours classified by?

A

Tumours are classified by: behaviour , histogenesis

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36
Q

What can behaviours be?

A

Behaviour - benign or malignant

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37
Q

What are benign behaviors?

A
  • localised (no BV invasion)
  • slow growing
  • well circumscribed
  • exophytic (outward growth)
  • rare ulceration + necrosis
  • close resemblance to normal tissue
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38
Q

What should you still remember by benign behaviours?

A

BUT can still be very pathological
- hormone secreting e.g. prolactinoma
- pressure on local structures e.g. pituitary -> optic chiasm
- obstruction
- transformation -> malignant

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39
Q

What are malignant behaviours?

A
  • BM invading
  • v-fast mitotic growth - hyper dense nuclei (stain dark)
  • poor circumscription (metastatic)
  • endophytic - inward growing
  • common necrosis + ulceration
  • poorly differentiated (little normal tissue resemblance)
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40
Q

What are malignant behaviors like?

A
  • pressure on structures
  • form 2 tumours
  • obstruction
  • very painful (often)
  • blood loss (often)
  • paraneoplastic e.g. SCLC (SIADH, Cushings)
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41
Q

What is histogenesis?

A

Origin of cell tumours

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42
Q

What is the histogenesis of epithelium?

A

Epithelium (carcinoma):
- non-glandular benign = papilloma
- non-glandular malignant = carcinoma (Basal cell carcinomas never metastises)

Glandular benign = adenoma
Glandular malignant = adenocarcinoma

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43
Q

What is the histogenesis of connective tissue?

A

Connective tissue (sarcoma) - adipocytes = lipoma, lipasarcoma
Muscle striated = rhabdomyoma, rhabdomoyosarcoma
Muscle smooth = leiomyoma, leuomyosarcoma
Cartilage = chondroma, choudrosarcoma
Bone = osteoma, osteosarcoma

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44
Q

What is the histogenesis of lymphoid?

A

Leukemia, lymphoma, (always malignant)

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45
Q

What are some other cancers?

A

Others: melanoma (melanocyte malignancy)
Mesothelioma (mesothelial malignancy - typically pleural)

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46
Q

What are some named cancers?

A

Names:
- burkitt’s lymphoma (B cell malignancy caused by EBV)
- Kaposi sarcoma (vascular endothelial malignancy, HIV associated)
- Ewing sarcoma (a bone malignancy)
- Teratoma (cancer of all 3 embryonic germ layers)

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47
Q

What are tumours graded on?

A

Similarity to parent cell:
1. Well differentiated (>75% cells resemble parent)
2. 10-75%
3. Poorly differentiated (<10% cells resemble parent)

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48
Q

What are characteristics of neoplastic cells?

A
  • Auto crime growth stimulation - overexpression of GF and mutation of tumour suppressor genes e.g. p53 and under expression of growth inhibitors
  • Evasion of apoptosis
  • telomerase; prevents telomeres shortening with each replication (this normally rate limits the extent of mitosis a single cell can undergo)
  • sustained angiogenesis + ability to invade BM
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49
Q

What are characteristics of neoplastic cells?

A
  • Auto crime growth stimulation - overexpression of GF and mutation of tumour suppressor genes e.g. p53 and under expression of growth inhibitors
  • Evasion of apoptosis
  • telomerase; prevents telomeres shortening with each replication (this normally rate limits the extent of mitosis a single cell can undergo)
  • sustained angiogenesis + ability to invade BM
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50
Q

What are the classes of carcinogens (cancer-causing agents)?

A
  • chemical e.g. paints/dyes/rubber/soot
  • viruses - EBV (burkitts), HPV (cervical cancer)
  • ionising + non ionising radiation - UVB in skin cancer, ionising in lots!
  • hormones, parasites, mycotoxins - e.g. increased oestrogen implicated in breast cancer
  • misc - e.g. asbestos
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51
Q

Difference between germline and somatic mutations?

A

Germline vs somatic mutations:

  • germline = mutated original germ cell -> will pass onto next gen
  • somatic = mutated mitotic copy of germ cell -> wont pass to next gen
52
Q

What is the pathway of metastasis?

A
  1. Detachment (from 1)
  2. Invasion of other tissue
  3. Invasation of BV
  4. Evasion of host defence, adherence to BV wall
  5. Extravasation to distant site
53
Q

What are the methods of spread?

A

Haematogenous -> via blood. Bone, breast, lung, liver

5 main mets to bone = BLTKP; breast, lung, thyroid, kidney, prostate

Lymphatic -> 2 formation in lymph nodes
E.g. lymphoma (rubbery lymphadenopathy)

Transcolemic -> via exudative fluid accumulation, spread through pleural, pericardial + peritoneal effusions

54
Q

What is the method of spread for sarcomas and carcinomas?

A

Sarcomas - mostly haematogenous
Carcinomas - mostly lymphatic

55
Q

What are exceptions to carcinomas mostly lymphatic transmission?

A

Follicular thyroid
Chanocarcinoma
RCC
HCC

Ft CRH?

56
Q

What are staging tumours?

A
  • mostly TNM (tumour - node - metastases)
  • different for leukemias + lymphomas and CNS cancers e.g. lymphoma -> ann arbour 1-4, A or B
57
Q

What mutations are involved in colorectal cancer?

A

Mutation involved in colorectal cancer
- FAP (familial adenomatous polyposis) -> autosomal dominant mutated APC gene (adenomatous polypasis coli), millions of colorectal adeiamas. Inevitable adenonoaroma by 35 y/o overexpression of c-mYC and point mutation in KRAS

  • HNPCC (lynch syndrome) -> mutated MSH gene, autosomal dominant; this genes involved in DNA mismatch repair
58
Q

What is screening?

A
  • method of early detection (essentially 2 prevention, making management easy!)
  • cancers screen for in UK = cervical (cervical swab), breast (mammogram), colorectal (fecal occult)
  • heel prick test at birth (Sickle cell, CF, hypothyroid)
59
Q

What are dendritic cell?

A
  • APC
  • of mesenchymal origin (not haematopeitic)
60
Q

What cells are involved in innate immunity?

A

Eosinophils (parasites)
Basophil (allergy)

Innate immunity:
Neutrophils
Macrophage

61
Q

What are cells of adaptive immunity?

A

NK cell
T cell
B cell
Plasma cell

62
Q

What are lymphoid organs?

A

1 - bone marrow - all cells originate, B cell mature
Thymes - T cell maturation + ‘thematic tolerance’

2- lymph nodes - APC + T/B cell interactions
Spleen - RBC recycling, encapsulated bacterial killing

(3 = pathological germ line centres of rapidly proliferating lymphocytes)

63
Q

What is innate immunity?

A

Non specific, rapid, already active (little activation needed), no memory
Killing usually: complement activation
Neutrophil + macrophage mostly

Physical barriers - skin, mucus, cilia
Chemical barriers - lysozyme in teas, stomach acid

64
Q

What is the complement system?

A

Destroy foreign antigens by
- direct lysis -> membrane attach complex formation (MAC)
- organisation -> increased phagocytosis (c3b)
- inflammation -> macrophage chemotaxis (c3a + cSa)

65
Q

What are the pathways of complement system?

A
  • classical
  • lectin
  • alternate
66
Q

What are neutrophils?

A

70% all WBC, hours-days, express CD66 receptor (common for all granulocytes)
Key mediator of acute inflammation
F -> essentially mini bombs of N.E, MPO and other ROS

“Polymorphs” = variable number lobes of nucleus

67
Q

What are macrophages?

A

Months- years. Can be circulating or resident (e.g. kuppfer)
Clear apoptotic debris
Have TLRs, complement receptor and AB’s bound Fc component

68
Q

What are eosinophils?

A

Contain MBP, often seen in parasitic infection

69
Q

What are basophils + mast cell?

A

IgE binding -> degranulation -> histamine release. T1 hypersensitivism M?
Mast cells = fixed at tissues
Basophil - circulating in body

70
Q

What are basophils + mast cell?

A

IgE binding -> degranulation -> histamine release. T1 hypersensitivism M?
Mast cells = fixed at tissues
Basophil - circulating in body

71
Q

What are NK cells?

A

Key role in (self cell killing) viral cell killing; activation + malignant cell killing = degranulation -> perforin (perforates viral infected cells)

(Essentially lymphoid cell)

Natural killer - kills natural host cells

72
Q

What are receptors on these cells (against pathogens?)?

A

Toll like receptors (vs pathogens?) + nodule like receptors

(Non Cell bound receptors, free in blood = lectins)

These respond to PAMPs - pathogen associated molecular patterns
DAMPs - damage

73
Q

What are TLRs composed of?

A

2 - detects growth (+) and TB
3 - intracellular
4 - LPS (-)
5 - flagellin
7 - single strand RNA intracellular
8 - ultra cellular
9 - non-myelinated DNA

74
Q

Where are TLRs?

A

3,7,8,9 are intracellular
Rest are on CSM (extracellular)

75
Q

Give an example of how TLR works?

A

TLR-4 activated by LPS of gram -ve bacteria (endotoxin)
Lectins in bloodstream bind pathogen
Then trigger immune response
- active complement, stimulate cytokines release (TNF a, IL1, IL6)
Increased phagocytosis

76
Q

What do antigen presenting cells do?

A

Interface between innate bad adaptive immunity

Best cells - dendritic cells
They present foreign antigens to Th cells:
- stimulates further Th proliferation
- stimulates B cell production -> antibodies

77
Q

What forms an immmne synapse?

A

When dendritic cell and Th cells communicate

78
Q

What conditions must be met for an immune synapse to function?

A
  1. Receptor binding
  2. Co-stimulation (other molecules bind after primary receptor binding)
  3. Cytokine release
79
Q

What conditions must be met for an immune synapse to function?

A
  1. Receptor binding
  2. Co-stimulation (other molecules bind after primary receptor binding)
  3. Cytokine release
80
Q

What other cells can be antigen presenting cells?

A

E.g. macrophage, B cells but dendritic are the best

81
Q

What is adaptive immunity like?

A

Specific, slow, need activation, have memory
Killing usually, antibody mediated
Main cells are T + B (+plasma) cell

82
Q

What are T cells like?

A

Maturation in thymus (after BM production)

Thymus tolerance chooses which T cells are good

83
Q

How does thymic tolerance work?

A

+ve selection -> T cells tested to see if they recognise thymus’ MHC’s 1+2; selected FDR
-ve selection -> if T cells produce immune response = selected against
- allocation - if T cells interacted with MHC 1 -> CD8 + cells (Tc)
MHC2 ->CD4 + cells (TH)

84
Q

What is a naive T cell?

A

T cell never encountering antigen (not matured in thymus yet)

85
Q

What does CD8+ do?

A

Interacts with MHC1
F = cytotoxic killing

  1. Perforin secretion (mediated by granzyme B)
  2. Express Fas L -> activates caspases
86
Q

What does CD4+ do?

A

Interacts with MHC2
2 types: TH1 = IFNY - activates NK cells and macrophages ( increased innate response)
TH2 = IL4 -> activate B cells to differentiate into plasma cells (increased adaptive response)

87
Q

What else is in adaptive immunity?

A

T regulatory (IL10) - immune tolerance
and TH17 - inflammatory at mucosal membranes

88
Q

What are B cells like?

A

Maturation and production in BM (B cells that launch immunity vs self - adaptive here)

CD19 and CD20 receptors

89
Q

How are B cells activated?

A
  1. They are activated by APC binding + MHC 2 interaction (e.g. with dendritic cell)
  2. TH 2 releases - IL4 which induces B cell proliferation (clonal expansion)
    - IL5 which induces B cell differentiation into plasma cell (produce GRAMED Ig’s)
90
Q

How do Ig’s act?

A

Ig’s act against specific pathogen present but if need arises:(e.g. pathogen antigens are very strange), AID (activation induced cysteane deamilase) can:

A: produce point mutation in Ig as “evolutionary” measure; somatic hypermutation
B: induce class switching (mutate are GAMED -> another isotype)

91
Q

Give examples of class switching

A

IL4 promotes class switching to IgA
IL5 promotes class switching to IgE (e.g. in allergic response

92
Q

What are the different types of immunoglobulins?

A

IgA,M,E,D

93
Q

What is IgG like?

A

Most abundant immunoglobulin in blood
Key in secondary immune response (this marker of immunological memory), v. Specific
Ig (mc-1)1,2,3,4 subtypes

94
Q

What is IgA like?

A

Most abundant Ig in total body
Found on mucosal linings + in colostrum/breast milk
Forms dimer

95
Q

What is IgM like?

A

First Ig released in adaptive response, less specific
Forms pentamer

96
Q

What is IgE like?

A

Activates mast cell + basophil degranulation in T1 hypersensitivity
(Anaphylaxis)

97
Q

What is IgD like?

A

Unknown function, presumed to be B cell receptor components?

98
Q

What are MHCs?

A

Major histocompatibility complex, on chromosome 6, aka HLA molecule

99
Q

What are MHCs?

A

Major histocompatibility complex, on chromosome 6, aka HLA molecule

100
Q

What are the key functions of MHCs?

A

Key functions:
1. interactions with T cells; TH (CD4+) interact with MHC2 (on APCs), TC (CD8+) interact with MHC1 (on all nucleated cells)(therefore not RBC!)

These essentially ensue the T cells confer immunity vs specific antigen while recognising self cells (APCs)

  1. Confer susceptibility to inherited autoimmune diseases e.g. HLAB27 -> spondyloarthropathies
    HLADR2 DQ3 -> TiDM
    HLADQ2/DQ8 -> coeliacs
    HLAB8 -> SLE
101
Q

What is Type 1 Hypersensitivity like?

A

Type 1 Anaphylaxis IgE mediated
- IgE binds to basophil/mast cell->.degranulation -> histamine; vasodilation + increased permeability (H1 receptor), bronchoconstriction, facial flush, purities, swollen tongue + face

E.g. ATOPY - asthma, hayfever, arthritis,

102
Q

What is Type 2 hYPERSENITIVITY LIKE?

A

Antigen-antibody complex
- IgG/M binds to antigen + activates MAC (Complement) at site of A-A binding
- e.g. goodpasture’s, AIHA, pernicious anemia, rheumatic fever

103
Q

What is Type 3 Hypersensitivity like?

A

Immune complex deposition
- IgG/IgA binds top antigen + activates complement at site of A-A deposition (kidneys = big boy affected)
- e.g. SLE (including lupus nephritis), post strep glomerulonephritis, IgA glomerulonephritis

104
Q

What is Type 4 hypersensitivity?

A

T cell mediated
- TH1 activated by APCs -> response
- e.g. DMT1, TB, MS, Guillain barre

105
Q

What is anaphylaxis?

A

Acute medical emergency
- may present with anaphylactic shock (sever hypotension, tachycardic + dyspnoea/cannotase, pale, cold extremities, puffed up face = tongue, itching -> purities, central cyanosis)

106
Q

How do you respond to anaphylaxis?

A

Tx 1 - ABCDE: asses vitals

Airway - can they breathe (airway patent)
Breathing -> is it rapid, wheezy, SpO2 <92%
Circulation -> are they pale, cold, clammy, decreased BP
Disability -> confused/camatose, movement
Exposure

2- ASAP treat with 500mg IM Adrenaline
- if necessary, consider - antihistamine (Chloratrenamine), cortisol (hydrocortisone)

107
Q

What is immune tolerance?

A

= physiological (to prevent frailty T/B cell self response)
- central -> thymic tolerance
- peripheral -> if T/B faulty cell evade central tolerance , they’re dealt with in 2 lymphoid organs (e.g. spleen)

108
Q

What is autoimmunity?

A

Pathological response vs self; faulty immune tolerance; or molecular mimicking

Organ specific (affect main organ)
- T1DM -> endocrine pancreas -> B cells
- MS -> oligodendrocytes of CNS
- pernicious anemia -> parental cells of stomach
- Hashimotoy -> anti-TPO Ab; thyroiditis

TSH-R -> graves
Ach-R Ab’s -> MG

109
Q

What is the Non-organ specific autoimmunity?

A

Generalised effect

-> affects DNA; ANA in SLE
-> affects cell antigens;
- RBCs -> autoimmune haemolytic anemia
- Platelets -> immune thrombocytic purpura

-> RA

110
Q

How does one become immunodeficiency?

A
  • can be:
  • inherited (defects in T cells) e.g. IgA (Mc in north Europe) deficiency, SCID (death within 2y)
  • acquired (HIV)
111
Q

What are the patterns of immunodeficiency?

A
  • Decreased CD4+ in HIV (these TH = required for cell mediated immunity; for both macrophage priming? and B cell activation)

Therefore increased susceptibility to disease e.g. CMV colitis (owl eyes), TB, pneumocystitis pneumonia, oral candidate, EBVKitt lymphoma’s

  • B cells may be deficient (decreased plasma cells = decreased Ab’s)
  • neutrophil + macrophage deficiency (required for phagocytosis + acute inflammation)
  • complement deficiency (needed for innate immune killing of bacteria associated with SLE)
  • Hyposplenism (lack of / decreased function of spleen; RNC recycling + killing encapsulated bacteria -> s.pneumo, N.meningitis, H.influenza)
112
Q

What are vaccinations?

A

A form of artificial active immunity - usually 2 doses; prime, then booster
Can be: - live attenuated (GM) organism e.g. MMR
- antigens
- toxins - e.g. tetanus
- CW constituents e.g. HepB

Trigger immune response top mimic natural infection without being symptomatic
1. initial IgM Ab’s made
2. If pathogen encountered again IgG spike seen

113
Q

What are routes of administration?

A

Enteral (GIT involved e.g. oral/PO)
Paraentral (non-GIT; IM, IV, SV, SC injections)
With local or systemic effect

(+ inhaled - ICS
Topical - cream
Rectal - enemas, suppository)

114
Q

What are drug targets?

A

Mostly receptors

115
Q

What can ligands be?

A

Agonists or antagonists

Agonists- full affinity. ( how well it bonds), full efficacy ( how well receptors activated)

Antagonists- full affinity, zero efficacy

Most receptors are g-protein coupled receptors

116
Q

What is potency?

A

How well a drug works (strength) - how much drug is needed to elicit response in the body

117
Q

How do agonists bind?

A

Direct binding

118
Q

How do antagonists bind?

A

Competitively (compete for active site) or non competitively (allosteric) inhibit receptors

Direct binding

Competitive antagonists decreases potency but doesn’t affect efficacy
- ligand co centration is rate limiting

Non-competitive antagonist decreases both potency and+ efficacy
- ligand concentration not rate limiting here

119
Q

What are other types of receptor ligands?

A

Other than direct bonding

  • allosteric modulators; increase/decrease normal ligand binding e.g. benzodiazepine
120
Q

What can drugs be?

A

Selective or non-selective;

  • propanalol = non selective beta blocker -> binds both B, (heart) and B2 (lungs)
  • verapamil = selective beta blocker -> binds only B1 (heart)

And also Beta-adrenergic agonists;
- isoprenaline = non selective Beta agonist -> both B1 + B2 (increased contractility + bronchoconstriction)
- SAB2A = selective Beta 2 agonist -> only bronchodilation

121
Q

What are some other drug targets?

A

Enzymes, transporters, ion channels

122
Q

How do enzyme drug targets work?

A

Main examples are cox-1 and ACE-i
- NSAIDs inhibit cox-1; prevent arachidanic acid -> prostaglandins SE-> GI ulcers
- ACE-i inhibit angiotensin 1-> angiotensin 2 (antihypertensive) SE-> hyperkalaemia, dry cough, teratogenic

123
Q

How do enzyme drug targets work?

A

Main examples are cox-1 and ACE-i
- NSAIDs inhibit cox-1; prevent arachidanic acid -> prostaglandins SE-> GI ulcers
- ACE-i inhibit angiotensin 1-> angiotensin 2 (antihypertensive) SE-> hyperkalaemia, dry cough, teratogenic

124
Q

What are transporters like?

A

(Mostly ATP-dependent)
- PPI’s e.g. omeprazole -> irreversible inhibition of H+ - K+ ATPase pumps therefore decreased gastric pH
- diuretics - loop; inhibits NKCC2 symporter in ascending limb (furosemide)
- thiazides (bendroflumetheziade); inhibits NaCl cotransporter in D T
- spironolactione; K+ spanning diuretic; inhibits aldosterone action
-SSRI’s, TCAs

125
Q

What is the difference between specific vs selective drugs?

A

Specific - act on a certain target
Selective - acts on subtype of target e.g. cardioselective Bb inhibit B adrenoreceptors NOT B2

126
Q

What are pharmokinetics?

A

What happens to the drug in the body - ADME
1. Administration- route + entry into body
- bioavailability - how fast and to what extent drug reaches systemic circulation
- Iv = always 100%
- other routes compared to IV!

ICS Intro (2 decks)

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