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2a systems > ICS > Flashcards

ICS Flashcards

1
Q

cardinal signs of inflammation

A

rubor
calor
dolor
tumor
loss of function

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2
Q

main cells in acute and chronic inflammation

A

acute- neutrophils
chronic- macrophages and lymphocytes

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3
Q

what wbc is raised during viral infection

A

white blood cell

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4
Q

causes of acute inflammation

A

microbial infections
hypersensetivity
physical agents, trauma, heat/ cold
chemicals
bacterial toxins

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5
Q

causes of chronic inflammation

A

autoimmune condition
primary granulomatous disease
transplant rejection
necrotic tissue

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6
Q

stages of inflammation

A

increase in vessel calibre- vasodilation is mediated by bradykinin, prostacyclin, NO
fluid exudate- vessels get leaky and fluid is forced out
cellular exudate- wbc especially neutrophils leave vessels

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7
Q

neutrophil action in acute inflammatiomm

A

margination- to edge of bv
adhesion- selectins facilitate binding of neutrophil to endothelium- then roll along bv margin
emigration+ diapedisis- formation of cellular exudate when neut leaves bv, other rbc following it
chemotaxis- cells following cytokines to site of inflammation
@ site of inflam- phagocytosis, phagolysosome + bacteira killing, macrophages clear debris

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8
Q

outcomes of acute inflammation

A

resolution
supparation- puss
organisation- form granulation tissue or fibrotic tissue- cardiac tissue or neurons never resonve- may become this at best
progression to chronic

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9
Q

define granuloma

A

aggregate of epitheloid histocytes- baso a bunch of macrophages around central pathogen

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10
Q

granuloma + eosinophil

A

parasite

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11
Q

granulomas secrete what blood marker

A

ACE

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12
Q

examples of granulomatous diseases

A

tb, chrons, leprosy, sarcoidosis

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13
Q

thrombi definition

A

mass of blood constituents - mainly platelets- forming in vessels during life

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14
Q

stages of throbosis

A

1- vasospasm
2- primary platelet plug formation- vwf binds to exposedd collagen and then platelet binds to that and get activated. discoid- pseudopoid and platelets bind together
3- coagulaition cascade (intrisic is 12,11,9,8, extrrinsic 3,7,10) to make fibrin mesh
4- plasminogen- plasmin

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15
Q

what influences thrombosis

A

virchows triad
endotheliam injury - smoking, mi, trauma
hypercoagubility- sepsis, cancer, contraceptives
abnormal bloodflow- af, venous stasis

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16
Q

arterial thrombosis cause, pressure, made from, lead to, treatment

A

atherogenesis, high pressure
made of platelets
lead to mi or stroke
antiplatelets like aspirin

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17
Q

venous thrombosis cause , pressure, made from, lead to, treatment

A

venous stasis
low pressure
rbc
dvt/pe
anti-coagulants like warfarin or heparin

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18
Q

eg of an antiplatelet and anticoaguland

A

antiplatelet- aspirin
anticoagulant- warfarin, heparin

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19
Q

outcomes of thrombi

A

resolution- plasmin degrades clot
organization- forms scar tissue, cardiac/ neurons at best go back to this
embolism- fragments break off and lodge in distal circulation

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20
Q

ischaemia vs infarction

A

ischaemia- reduction in blood flow- cardiomyoctes and cerebral neurones most vunerable to this
infatction- reduction in blood flow so severe it leads to cellular deaths

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21
Q

what organs have dual blood supply and therefore r less suseptable to infarctiom

A

liver
brain
lungs

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22
Q

what can embolism in systemic circulation lead to

A

atrial fibrilation or ischemic stroke

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23
Q

what can venous embolism lead to

A

pulmonary embolism if it enters pulmonary artery

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24
Q

apoptosis definition

A

non inflammatory, programmed cell death- avoids damage to surrounding cells

chromatin ulaltered, cells shrink, organeles retained and cell surface membrane stays intact

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25
Q

what is p53

A

protein that detects dna damage and triggers apoptosis

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26
Q

apoptosis in cancer and hiv

A

cancer- dont apoptose when expected to
hiv- t helper cells apoptose

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27
Q

mechanisms of apoptosis

A

intrinsic- cytochrome c activates caspases
extrinsic- fas ligands or tnf ligands bind to cell surface receptors and activate caspases
cytotoxic– cytotoxic t cells release granzyme b- perforin- caspases

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28
Q

necrosis- def, where does it occur

A

inflammatory and traumatic cell death where large number of cells die due to external factor- infarction / frostbite
cells burst and organelles splurge out, chromatin mutation is likely

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29
Q

what is the main protein involved in apoptosis

A

caspases

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30
Q

hypertrophy

A

tissue increases in size bc cells get bigger- eg muscle cells

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31
Q

hyperplasia

A

tissue increases in size bc no. of cells increase via mitosis

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32
Q

atrophy

A

tissue sizs decreases bc number of cells or size of cell decreases

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33
Q

metaplasia

A

change from one type of cell to another

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34
Q

dysplasia

A

change of a differentiated cell type to a poorly differentiated type- usually a precancerous change

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35
Q

carcinogenesis definition

A

transformation of normal to neoplastic cell through permanent mutation

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36
Q

neoplasm definition

A

autonomous abnormal persistent new growth of tissue

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37
Q

a neoplasm can only happen to what type of cells

A

nucleated cells- eg not erythrocytes

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38
Q

what is a tumor

A

any abnormal swelling

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39
Q

what can tumours be classified by

A

behaviour or histogenesis

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40
Q

behavioral classification on tumor- benign

A

no bm invasion
slow growing- low mitotic activity
well circumsized
well differentiated

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41
Q

behavioural tumor classification- malignant

A

bm invasion
fast growing- high mitotic activity
poorly circumscribed
common ulceration/ necrosis
poorly differentiatedd- little resemblance to normal tissue

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42
Q

reason for adjuvent thrapy with cancer

A

micrometastases could still be present after tumor completely excised

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43
Q

papilloma

A

benign neoplasm of epithelial tissue

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44
Q

carcinoma

A

malignant neoplasm of epithelial tissue

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45
Q

adenoma

A

benign neoplasm of glandular tissue

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46
Q

adenocarcinoma

A

malignant neoplasm of glandular tissue

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47
Q

benign and malignant neoplasm of adipocytes

A

lipoma, liposarcoma

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48
Q

benign and malignant neoplasm of striated muscle

A

rhabdomyoma, rhabdomyosarcoma

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49
Q

benign and malignant neoplasm of smooth muscle

A

leiomyoma, leiomyosarcoma

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50
Q

benign and malignant neoplasm of cartilage

A

chondroma, chondrosarcoma

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51
Q

benign and malignant neoplasm of bone

A

osteoma, osteosarcoma

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52
Q

is a grade 1 or grade 3 tumor more differentiated

A

grade 1- well differentiated- most cells resemble parent cell
grade 2- some cells resemble parent
grade 3- poorly differentiated- most cells look nothing like parent

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53
Q

characteristics of neoplastic cells

A

autocrine growth stimulation- overexpress gh and underexpress growth inhibitors
mutation of tumour supression genes like p53
can evade apoptosis and escape immune surveillance
telomerase is prevented from shortening with each replication
sustained angiogenesis

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54
Q

classes of carcinogens

A

miscellaneous- asbestos
hormones, parasites, mycotoxins
ionizing+ non ionizing radiation
viruses
chemical

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55
Q

pathway of metastesis

A

detatchment from first cancer
invades other tissue
invades blood vessel- collagenases + cell motility
evades host defense + adheres bv wall- platelet aggregation, shed surface antigens, adhesion to other tumour cells
extravasation to distant site- adhesion receptors, collagenase, cell motility

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56
Q

how does cancer evade immune system

A

platelet aggregation- body doesnt see anything but harmful platelets
shedding antigens from cell surface- macrophages engulf this instead of cell
adhesion to other tumour cells- ones in center dont get eaten

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57
Q

angiogenesis promoting and inhibitng factors

A

vascular endothelial growth factors
basic fibroblast growth factor

angiostatin
endostatin
vasculostatin

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58
Q

method of spread for tumours

A

haematogenous- via blood- form secondary tumors in organs
lymphatic- secondary formation in lymph nodes
transcolemic- via exudate fluid acculiation (baso effusions)

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59
Q

5 main metastesis to bone

A

breat, lung, thyroid, kidney, prostate

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60
Q

tumours that spread to liver

A

pancreas, stomach, colon, carcinoid tumour of intestine

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61
Q

how do sarcomas usuallt spread

A

mostly haematogenous

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62
Q

how do carcinomas mainly spread

A

mainly lymphatic

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63
Q

main method to stage tumour

A

tnm- tumour, node, metastases

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64
Q

what type of prevention is screening

A

secondary prevention

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65
Q

cancers that are screened for in the uk

A

cervical- cervical swab
breast- mamogram
colorectal- faecal occult

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66
Q

cells that regenerate

A

hepatocytes, blood cells, skin epithelium, osteocytes

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67
Q

cells that dont regenerate

A

myocardial cells
neurones

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68
Q

what is the pluripotent stell cells which blood cells r formed from

A

haematocytoblast

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69
Q

which precursor are innate cells from

A

common myeloid progenitor - eosinophil, basophil, neutrophil,macrophage

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70
Q

what precursor are adaptive cells from

A

common lymphoid progenitor- b, t cells and nk cells

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71
Q

lymphoid organs and what happens in them

A

primary-
- bone marrow- b and t cells made and b cells mature
-thymus- t cell maturation

secondary
- lymph nodes- apc+ b and t cell interaction
-spleen- rbc recylcing

tertiary
- germinal center of rapidly proliferating lymphocytes- pathological

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72
Q

physical and chemical barriers of innate immunity

A

physical- skin, mucus, cilia
chemical- lysosyme in tears, stomach acid

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73
Q

polymorphonuclear leukocytes + mononuclear leukocytes

A

neutrophil, basophil, eosinophil (granulocytes)

mono= monocytes, lymphocytes (agranulocytes)

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74
Q

what cell is most commonly seen in parasitic infections

A

eosinophils

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75
Q

difference between basophils and mast cells

A

basophils circulate around the body
mast cells are fixed in tissues

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76
Q

phagocytic cells

A

macrophage
neutrophil
dendritic cell

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77
Q

what are compliments + what immune system is it part of

A

proteins that are secreted in the liver and need to be activated to be functional- part of innate response

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78
Q

modes of action for compliment system

A

classical- ab antigen complex binds to microbe
alternative- compliment binds to microbe
lectin- lectin binds to microbe

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79
Q

outcomes of compliment (how it kills)

A

direct lysis- membrane attack complex
chemotacix- c3a and c5a- recruit leukocytes to site of infection
opsonisation-c3b

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80
Q

what is tnf-a secreted by and involved in

A

prod by macrophages and activates macrophages- involved in inflammation

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81
Q

cytokines: inteferons

A

limits spread of viral infection

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82
Q

cytokines: colony stimulating factor

A

controls division and differentiation of bone marrow stem cells

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83
Q

what do chemokines do

A

direct movement of wbc from blood to tissue/ lymph organs

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84
Q

what is il4 involved in

A

allergies

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85
Q

what are tlrs and nlr

A

innate immune sensors that respond to pathogen or damage associated molecular patterns

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86
Q

tlr2

A

2- peptidoglycan on gram positive bacteria

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87
Q

tlr4

A

pamp= lipopolysacharide / endotoxin- gram negative bacteria

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88
Q

tlr 5

A

pamp= flagellin- on flagellated bacteria

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89
Q

tlr 9

A
  • pamp- dsDNA on viruses
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90
Q

tlr 3,7,8,9 present on

A

viruses

91
Q

membrane bound prr example

A

toll like receptor

92
Q

cytoplasmic prr example

A

nod like receptor

93
Q

examples of prr (these r outside of a cell)

A

scavenger receptor- lipids
c type lectin receptors
toll like receptors

94
Q

what r rig like receptors for

A

sense cytoplasmic viral rna and produce inteferons

95
Q

what are nod like receptors for

A

sense cytoplasmc bacterial pathogens and DAMPs

96
Q

why dont we recognise our own dna and rna in innate response

A

dna and rna are where prrs cant acess it

97
Q

is damp on your own cell or another

A

on ur own- eg dna damage

98
Q

types of apc + professional ones

A

dendritic cells, b cells, macrophages

99
Q

what do apcs do

A

stimulate further t helper cell proliferation
stimulate b cell production and proliferaiton

100
Q

cell mediated vs humoral response

A

cell mediated= intraceullar microbes- t cell
humoural- extracellular microbes- b cells

101
Q

whats a naive t cell

A

never encountered an antigen- not matured in thymus yet

102
Q

th1 vs th2

A

cause apc to phagocytose
th2- ab production

103
Q

what happens to t cells that recognize self

A

killed in foetal thymus

104
Q

il4 and il5 released by th2

A

4- clonal expansion
5- differention

105
Q

high levels of il12 do what

A

th1- t cell mediated
absence of this causes b cell

106
Q

how are t helper cells activated

A

apc binding and mhc interaction

107
Q

intrisic antigen triggers what mhc and what t cell

A

intrisic antigen binds to mhc 1- activates cd8 cell- kill infected cell

108
Q

extrinsic antigen- mhc and t cell

A

extrinsic- mhc class 2- cd4 cell- helo b cell make ab

109
Q

ch4 cells will interact with what mch

A

2

110
Q

cd4 cells will interact with what mhc

A

mhc1

111
Q

mhc 1 and 2 are found on what cell

A

1- on all nucleated cells
2- on apcs

112
Q

what do ab do

A

neutralise toxin by binding to it
increase opsonisation for phagocytosis
activate compliment

113
Q

what are ab usually secreted as

A

ig m- later class switch to igg but hve specificity to same antigen

114
Q

what is somatic hypermutation

A

point mutation of evolutionary measure- eg igs will mutate if u have a slightly different strain of covid

115
Q

what is the fc and fab region of anitbodies

A

fc- constant- self and binds to surface of wbc (big stick)
fab- antobody binding region- binds to epitope of antigen

116
Q

igg-

A

most abundant in blood
important in secondary immune response
crosses placenta

117
Q

iga

A

most abundant in body
in mucisal lining- colustrum and breastmilk

118
Q

igm

A

first released in adaptive response

119
Q

ige

A

activates mast cells and basophils

120
Q

type 1 hypersensetivity

A

anaphylaxis- ige mediated
ige binds to basophil or mast cell- degranulation- histamine (vasodilation and increased vessel permeability, bronchoconstriction, facial flush, swollen tongue and face)

121
Q

type 2 hypersensetivity

A

antigen-antibody complex- igg/igm binds to antigen and activates compliment at the site of a-a binding
eg- goodpastures, pernicious anemia, rheumatic fever

122
Q

type 3 hypersensitivity

A

immune complex deposition
igg/iga binds to antigen and activates compliment at the site of a-a deposition
eg- sle, post strep glomerulonephritis or iga glumerulonepohritis (affects kidney hard)

123
Q

type 4 hypersenstivity

A

t cell mediated, delayed response
eg dmt1, tb, ms, guillain barre

124
Q

what is immune tolerance, central tolerance and peripheral tolerance

A

immune tolerance is physiological to prevent faulty t/b cells self response
central tolerance is thymic tolerance where immature t cells are maturing and dealt with positively or negatively
peripheral tolerance occurs in secondary lymphoid organs and occur if faulty t/b cells evade thymic tolerancew

125
Q

when you get a vaccine what ab is initially made and what ig wwill be there when pathogen is encountered again

A

initially- igm
reencounter- igg

126
Q

natural active immunity

A

body encouonters pathogen and produces memory cells after infection

127
Q

artificial active immunity

A

vaccine mimics encountering a pathogen and stimulates ig production

128
Q

natural passive immunity

A

maternal igs passed onto feeding baby in breastmilk/ colostrum- no memory cells

129
Q

artificial passive immunity

A

antivenom (injection of ig from another organism)

130
Q

covid 19 vaccines are called what and what are they made of

A

pfizer and biotech moderna- made of mRNA

131
Q

define passive immunity and give advantages and disadvantages

A

short term results from introduction of antibodies from another person or animal
adv- immeadiate protection and effective in immunocompromised patients
disadv- short lived and no memory cells and possible transfer of pathogen

132
Q

define active immunity

A

antigenic substance prepared from acausative agent of disease- introduces pathogenic foriegn pathogens to trigger t lymphocytes, acp then b memory cell

133
Q

vaccines can be…

A

non living- whole killed, toxoids
living- live attenuated

134
Q

eg of whole killed vaccines- describe them and give advantage and disadvantage

A

influenza, rabies, sars-co-v2
doesnt cause infection byt contains antigen which produces immune response
adv- good for immunoconpromise and doest need to be refrigerated so can be transported
disadv0 need at least 2 shots, weaker response and lack of t cell response

135
Q

what are toxoids in vaccines

A

inactivated toxins

136
Q

what are live attenuated vaccines, examples and adv and disadv

A

organism is cultured in a way which it doesnt cause disease when innoculated; loss pathogenicity but kept antigenicity
eg bcg and mmr
adv- lower dose and less dose needed, immune response mimics that of real infection
disadv- transmissiability, vaccines need to be refreigerated so less transport

137
Q

what are old people vaccinated for

A

pneumococcal
influenza
covid-19

138
Q

what are routes of administration for drugs for systemic and local effects

A

sysmtemic:
- enteral (gi tract involved- per oral/ per rectal)
-parenteral (non gi tract- im, iv, subcutaneous)
local:
- inhaled
- topical (cream)

139
Q

eg of drug targets

A

mostly receptors- also enzymes (ace i), ion channels, membrane transporters

140
Q

what is a ligand- exogenous and endogenous

A

anything that binds to a receptor
- exogenous is drugs, endogenous is hormones

141
Q

what is an agonist and antagonist

A

agonist- full affinity (binds) and full efficiacy (activates receptor to reach a response)

antagonist- full affinity but no efficiacy- binds but doesnt activates

142
Q

a full agonist and inverse agonist and antagonist will produce what response

A

full agonist-100% response
inverse agonist- priduce effect opposite to agonist
antagonist- no effect of its own, just blocks effect s of agonist

143
Q

what do u call the strength of a drug

A

potency

144
Q

eg of ligand gated receptor, nuclear receptor, kinase linked receptor

A

ligand gated- ach receptor
nuclear- steroid receptor
kinase linked- growth factor (catalyse transfer of phosphate between proteins)

145
Q

what happens when a ligand binds to a g protein receptor

A

gdp turns into gtp

146
Q

draw a graph of agonist and competetive and non competetive antagonists

A

on notes

147
Q

what does it mean if a beta blocker is non selective

A

itll bind to both b1 and b2 receptors

148
Q

how do nsaids work

A

inhibit cox-1- reduction in prostaglandins which are important for maintaining healthy gi mucosa

149
Q

what does cox 1 inhibition do

A

decrease gastric mucosal protection so decreases stomach ph and have a risk of gastropathy

150
Q

what does cox-2 inhibition do

A

anti-inflammatory (cox-2 is involved in inflammation)

151
Q

what does aspirin irreversibly inhibit

A

cox-1 - its an nsaid

152
Q

eg of a ppi and what it does

A

omeprazole
irreversibly inhibits h-k atpase pumps- increases gastric ph to make it less acidic

153
Q

what is pharamacokinetics

A

what happens to the drug inside the body
ADME

154
Q

breifly describe pharmacokinetics

A

administration- route and entry into body- iv, im… bioavailability is important here

distribution- how well a drug is distributed from plasma into intersitial fluid and intracellular fluid and fat. volume of distribution is important here and consider if it can cross bbb.

metabolism- by kudney and liver, classified by rate and phase
phase 1- microsomal enzymes ad an oh group and theres a slight increase in hydrophulicty
phase 2- conjugation- major increase

excretion- urine and faeces

155
Q

what si bioavailability and what has 100% bioavailability and why

A

how fast and to what extent a drug recaches systemic circulation
gold standard is iv as it avoids first pass metabolism (metabolised by kiver or gut first before site of action)

156
Q

pharmacokinetics- what affects how well a drug will be absorbed

A

lipid solubility- if more soluble, more will be absorbed
drug ionisation- if ionised, less will be absorbed

157
Q

pharmacokinetics- what is a high volume of distribution and a low one

A

if well distributed- high vd
if poorly distributed- low vd

158
Q

when can drugs cross the bbb

A

if bery lipid soluble, intrathecal administration, if inflammation is present making barrier leakyq

159
Q

pharmacokinetics- what things affect drug distribution

A

hydrophilipity- if its hydrophillic itll be poorer distributed
lipophillicity- if lipophilic better distributed
smaller molec- more distributed
protein bound- less distribution cuz its stuck to one protein

160
Q

pharmacokinetics- metabolism. what does the liver and kidney metabolise

A

kidney- smaller, water soluble molecules- pee
liver- larger hydrophobic molec- poo

161
Q

pharmacokinetics- metabolism- phase 1 and 2

A

1- slight increase in hydrophilicity via microsomal enzymes - CYP450
2- major increase in hydrophilicty by conjugation

162
Q

pharmacokinetics- what affects metabolism

A

cyp450 inducer and inhibitor drugs
inducer will increase metabolism- may result in sub theraputic dose
inhibition will decrease metabolism- may result in toxicity

163
Q

what is pharmacodynamics

A

effect a drug has on the body

164
Q

what is a drugs half life dependant on

A

clearance and vd (small vd is poorly distributed and cleared quicker)

165
Q

when is a drug considered to be cleared

A

5x half life

166
Q

what is steady state

A

rate of drug input= rate of drug elimination- between maximum safe concentration and minimim effective concentration

167
Q

what do you give if time taken to reach steady state is too long

A

give a loading dose

168
Q

nt and receptors for autonomic sympathetic nervous system

A

ach- nicotinic receot–noradrenalin to adrenerigic receptor

169
Q

nt and receptors for autonomic parasympathetic nervous system

A

ach- nicotinic receptor—ach to musacrinic ach receptor

170
Q

what are the ach receptors and where are the m ones found

A

cholinergic receptors which are muscarinic or nicotinic

m1- brain- cognitive processes
m2- decrease rate and force of heart
m3- smooth muscle contraction- mainly bladder

171
Q

what does botulinum toxin do

A

inhibits ach release- paralysis- used in cosmetics

172
Q

results of overstumulation of ach at nmj junction

A

cholinergic crisis- SLUDGE
salivation
lacrimation
urination
defication
gi distress
emesis- vomiting

173
Q

formation of adrenaline

A

tyrosine- L dopa- dopamine- noradrenalin- adrenalin

174
Q

Nad receptors

A

a1- vasocontriction + bladder contraction
a2- negative feedback
b1- increase heart rate and contractility
b2- bronchodulation

175
Q

eg of a1 antagonist and whys it important

A

tamsulosin- effects prostate and bladder- therefore treates benign prostatic hypertrophy - relaxes smooth muscle in prostate and detrusor in bladder

176
Q

eg of b2 agonist

A

salbutamon
saba+ laba

177
Q

give an example of a non selevtive beta blocker antagonist

A

propanolol

178
Q

what is a beta 2 antagonist

A

non selective beta blockers like propanolol

179
Q

where should adverse drug reactions be reported to

A

MHRA yellow card scheme

180
Q

what increases your risk of adverse drug reactions

A

reduced renal or hepatic clearance
polypharmacy

181
Q

what are the adverse drug reactions (eg and details in notes)

A

augmented-common, ecaggerated effect of drugs pharmacology
bizzare- not related to drugs pharmacology- eg allergy of anaphylacitc shock after penecilin
chronic- adr stays after drug is stopped
delayed- adr developed after a while
end of use- developes after drug stoppedd

182
Q

what is excretion effected by

A

urine ph- acids cleared fastier in weakly basic urine and vice versa

183
Q

what are naturally occuring opiods

A

morphine and codeine

184
Q

what is the modified version of morphone and how strong is it

A

diamorphine- heroin. 2x stronger than morphine

185
Q

oral bioavailibity of morphine

A

50%

186
Q

for 10 mg of diamorphine/ heroin how much morphine do you need/

A

5mg

187
Q

side effects of opiods like morphine

A

addiction
gi- constipation, n+v
resp- resp distress/ depression
(receptors found in cns and git and resp centers)

188
Q

what is the treatment for opioid induced resp depression

A

naloxone- comp opiod inhibitor.
- it has a short half life so beware of overdose

189
Q

what is tolerance vs dependance

A

tolerance- due to overstimulation of opiod receptor so you need more of the dose to acheive the same effect
dependance is psychological state of craving that eurphoria

190
Q

eg of antiplatlet drug

A

aspirin

191
Q

eg of anticoagulants- 2

A

heparin and warfarin

192
Q

what is warfarin and if patient is bleeding out on this drug what do you do

A

anticoag- antivitamin k- i fbleeding out give vit k

193
Q

dry cough is a common se of which drug

A

ace inhibitors

194
Q

diuretics

A

loop diuretic- furosemide. inhibits nkcc2 channel in ascending loh so more na, water, cl and k is excreted

thiazides- bendroflumethiazide- inhibits nacl cotransptter in dct so more na and cl and water is excreted

spironolactone- inhibts enac channel(aldosterone) - in collecting duct so more na, water excreted. k+ is spared

195
Q

what are the 3 layers of the normal artery wall and describe them

A

tunica intima- 1 endothelial layer thick
tunica media- smooth muscle (support and diameter), collagen, elastin (stretch and recoil to accommodate changes in blood pressure)
adventitia- connective tissue, collagen, nerve fibers and vasa vasorium

196
Q

difference between elastic and muscular arteries

A

elastic- closer to heart, more elastin in media to withstand higher pressure
muscular- further from heart- more muscle in media to vasoconstrict/ dilate

197
Q

define arteriole

A

less than 3 smooth muscle layers in media- site of greatest tpr

198
Q

what do branches of the rca supply

A

branches to san + avn
right marginal artery for inferior border of the heart
piv- both ventricles

199
Q

what do branches of the lca supply

A

left main stem branches into cx and lad
cx- inferior border, left atrium and ventricle, part of right ventricle
lad- both ventricles
cx branches into left marginal- left ventricle

200
Q

explain process of atherogenesis

A

1- endothelial injury- high bp, smoking, inflammation.. damage endothelium making it more permeable to lipids
2- ldl cholesterol penetrates arterial wall and accumulates. becomes oxidised and more toxic, macrophages engulf these and becomes foam cells
foam cells recruit other inflammatory cells like neut+ lymphocytes
3- fatty streak formation- foam cells + smooth muscle
4- fibroblasts produce fibrous cap over plaque
5- non ruptured= stable ruptured= unstable- continuous platelet plug and lumen occlusion

201
Q

modifiable risk factors for atherosclerosis + why theyre issues

A

smoking- releases nicotine and co- damages endothelium
hypertension- increases pressure damages bv wall
obesity
lack of excersize- helps bp
high cholesterol- more ldl - cuz of processes food

202
Q

non modifiable risk factors for atherosclerosis

A

age
sex- m
family history
t1 diabetes (increases glucose and free radicals)
ethnicity

203
Q

primary, secondary and tertiary prevention for atherosclerosis

A

primary- (prevent)- excersize more, change diet to less salt and sugar, stop smoking
secondary- statin to lower ldl, antihypertensives like acei, social prescribing like gym voucher
tertiary- surgical intervention- stenting, bypass to make new pathway for blood to flow around blocked artery

204
Q

what do you treat angina from atherosclerosis with

A

gtn spray sublingualy

205
Q

what is anaphylaxis

A

form of t1 hypersensitivity- acute allergic reaction to an antigen the body hypersensetive too and its severe and life threatening- have to have eithte airway or breathing or circulation propblems associated with skin or mucosal changes

206
Q

explain pathophysiology of anaphylaxis

A

1- sensitization- first exposure to antigen- antigen gets picked up by apc- presented to t helper cell- activates b cell- plasma cell- antibodies
il4 will cause b cells to class switch to igE
ige will bind to Fc receptor on mast cells and basophils

2- 2nd exposure- on reexposure of the antigen- antigen will form cross links on igE on mast cells- causes rapid degranulation of mast cells- leukotrines, trypases, histamine- will cause signs and symptoms

207
Q

presentation of anaphylaxis

A

occurs within minutes
vasodilation, bronchospasm, utricaria, increased vascular permeability
angioedema
central cyanosis
tachycardia, macroglossa, hypotension (due to vascular permeability, will compensate by raising bp)
wheezing (due to bronchoconstriction due to inflammation and increased vascular permeability)

208
Q

treatment of anaphylaxis

A

abcde (remove airways obstruction and traces of allergens like iv, check for bronchospasm like wheezing, colour pulse, responding)
call for help!!!!!!!!!
lay flat and raise legs

ADRENALINE 500 MICROGRAMS IM

give high flow o2 and iv fluid

209
Q

what does adrenaline do

A

stimulates beta 1 and 2 adrenoreceptors- positive ionotropic and chronotropic effect and lowers eodema and bronchodilates)

210
Q

why do you sometimes need to give a second dose of adrenalin

A

adrenalin has a short half life

211
Q

factors linked to an increase in allergies

A

increase in air pollution
change in pollen patterns
increase in caesarian sections- not exposed to microbiomes in vagi
contrasting agents- like x rays

212
Q

what qualities does a drug need to have to induce anesthesia quickly and why

A

low protein binding (increases plasma concentration) and high lipid solubility (readily crosses bbb)

213
Q

do you give iv or volatalile gas anasthesia first and why

A

iv- because iv drug has high initial plasma concentration - lots to well perfused area like the brain– but then spread to less perfused areas anc conc will decrease

214
Q

is a competetive and non competetive antagonist reversible or not

A

competetive is reversible but non competetive is irreversible

215
Q

most significant risk factor for atherosclerosis

A

hypercholesterimiea

216
Q

how does aspirin work (mode of action)

A

irreversibly inhibits COX to prevent breakdown of arachidonic acid into prostaglandin H2
its non selective for cox 1 and 2

217
Q

what is clopidogrel

A

anti- platelet drug

218
Q

what confirms the diagnosis of tb and what would you see

A

zeehl neilsen staining- appears as a red rod

219
Q

what do you do asap if you suspect meningitis

A

single STAT dose of benzylpenicillin by gp before transfer to hospital

220
Q

what is legionella pneumonia associated with

A

travel to spain
exposure to damp

221
Q

c difficile bacteria is spread through hosptialised pt. what is it usually caused by

A

c antibiotics- clindamycin, co amoxiclav, cephalosparins

222
Q

what is the sight campain to prevent spread of c difficile bacteria

A

suspect
isolate
gloves + apron in pt zone
hand washing b4 and after pt env
test stool for c difficile

223
Q

cranial and nephrogenic di water deprevation results

A

cranial- after fluid dep low urine osmolality but high after desmopressin

neph- low for both bc kidney doesnt respond

224
Q

what is the tumour supression gene

A

p53

2a systems (7 decks)

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