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Year 2 > Unit 4 > Flashcards

Unit 4 Flashcards

1
Q

Taste receptor for umami

A

T1R1 T1R3

l-glutamate

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2
Q

Taste receptor for sweet

A

T1R2 T1R3

sugars, glycine + d amino acids

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3
Q

Taste receptor for bitter

A

30 T2R

Cycloheximide

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4
Q

Taste receptor for sodium

A

ENaC

NaCl

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5
Q

Taste receptor for sour

A

PKd2L1 acids

CA IV
carbonated drinks

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6
Q

Routes malignancy

A

Blood
lymphatics
local
transcoelomic - peritoneal cavity

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7
Q

HER 2

A

ONCA-GENE

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8
Q

BRACA 1/2

A

TSG

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9
Q

Innervation tongue paillae

A

Circumvallate – IX
Foliate – VII + IX
Filiform – VII
Fungiform – VII

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10
Q

Describe how viruses cause cancer?

A

Virus can directly encode viral oncogene= viral oncogenesis. Or active proto-oncogenes inside cell. Tumour viruses (both DNA + RNA) interact with OG + TSG + transition from infection to cancer depends on the “genetic background” of the infected cell.

RSV carries viral oncogenes + inserts them directly into host genome.

ALV activates existing proto-oncogenes in host cells via insertional mutagenesis.

Others inactivate TSG -> HPV. Viral promoters which drive protein expression within the host cell.

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11
Q

What is the Rous Sarcoma Virus and how does it work?

A

Retrovirus with ssRNA genome. RSV has transforming potential via a single gene v-src (viral sarcoma) which incorporates into host cell genome. Transforming potential passes between generations.

V-src encodes a constitutively (always active) active tyrosine kinase + infected cells unable regulate v-src activity as its always active * has ability to stimulate host of cellular pathways. V-src DNA sequence similar to gene in non-cancerous cells = cellular-src.

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12
Q

How ALV became viral oncagene

A

ALV infected a cell its ds DNA was integrated into host cell genome-this is completely random in one infection the ALV virus sat next to c-src – as virus transcribed viral DNA it took with portion of c-SRC and packed into virus and ALV become a different virus which carriers a copy of this viral oncogene.

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13
Q

why not all cells infected ALV become tumours

A

In the first three examples the virus has integrated upstream of non-critical genes * effect host cell may see overexpression of these genes but not cancerous as no proliferative advantage. In cells that go onto form leukaemia the cell integrates directly upstream of myc * lots of TF * cell proliferates uncontrollable. This explains slow tumour formation as need millions and millions of insertion events after being infected with the virus for viral DNA to insert directly upstream of myc.

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14
Q

How lesion V3 affects ear

A

v3 innervates tensor tympani * lesion get hyperacusis cant dampen loud sounds

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15
Q

joints name ossicles

A

synovial

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16
Q

Joint name stapies

A

ball + socket

17
Q

Innervation stapedius

A

facial nerve

18
Q

Innervation tensor tympnai

A

V3 division trigeminal

19
Q

Visual pathway

A

Inner hair cells connected type 1 spiral ganglion - cochlear nerve to cochlear nucleus
moss cross collaterally and synapse superior olivary nucleus.
Travel down lateral lemiscus to inferior colliculus - medial geniculate nucleus

20
Q

Why not all cells infected ALV form tumours

A

If virus integrats upstream of non-critical genes * effect host cell may see overexpression but not cancerous as no proliferative advantage.

Leukaemia the cell integrates directly upstream of myc * lots of TF * cell proliferates uncontrollable. This explains slow tumour formation as need millions and millions of insertion events after being infected with the virus for viral DNA to insert directly upstream of myc.

21
Q

How HPV 16 /18 creates tumour

A

HPV16/18 produces viral proteins e6 and e7 which inhibit actions of important TSG in infected cells. E7 inactivates Rb proteins * disrupts cell cycle progression control. E6 marks P53 for degradation * reduced p53 levels in infected cells.

22
Q

how cells get immortality

A

express telomerase reverse transcriptase (hTERT)

23
Q

6 step metastasis

A 
Local invasion - EMT
Intravasation - lymph/ BV
transport
Extravsation 
Micro mets -MET
Colonisation + macromets
24
Q

Neoplasm: .

A

mass of cells with uncoordinated growth and complete or partial loss of the normal growth control mechanisms

25
Q

Dev invasive carcinoma

A
  • Dysplasia: some abnormal cell growth/ some but not all cytological features of carcinoma in situ + confined by BM
  • Carcinoma in situ: all hallmarks invasive carcinoma (neoplasia) but confined BM at this point IT DOENT HAVE METASTATIC POTENTIAL

• Invasive carcinoma: breaches BM. Carcinoma In-Situ will progress to invasive then metastatic if left untreated. Carcinoma in situ is common in epithelial – cervix, breast, colon + skin.

26
Q

SIRS to sepsis

A

PBMC -> TNF alpha - feedback loop TF expression, neutrophil activation + NO production.

TNF aplha activates endo cells - endo cells - TF (coagulation)/NO (capillary leakage).
TNF alpha activates blood neutrophils -> TNF alpha -> NETS

Severe non localised oedema, poor perfusion tissues, hyper coagulation
-> organ dysfunction

27
Q

CARS

A

Compensatory anti inflam response syndrome

Increase TGFB + Il-10
Downreg TNF alpha, CXCL8 + NO.

Run out cells + cnat make more as bone marrow hypoperfused - as dont have many inflam cells body assumes infection over - no longer presenting pathogen getting type 1 reposnce. Get sudden improvemnt followed by drop off

28
Q

Sepsis organisms

A

Eschericia coli

Staph aureus

29
Q

Sepsis 6

A

Complete 1 hour - double patients chance survival

Administer high flow oxygen
Take blood cultures
Broad spec AB
IV fluid
Serum lactate + heamoglobin
Accurate hourly urine output
30
Q

Sepsis from SIRS

A

Increase TF - hypercogulation - depletion clotting factors - increased anticogulation. Hypoperfusion, coagulation + ROS cause direct organ damage

31
Q

Septic shock

A

Increase TF - hypercogulation - depletion clotting factors - increased anticogulation -> low BP/ MAP.

SIRS - Increase TNF alpha, Oedema + hypoperfusion - low BP/MAP

32
Q

Pathogens meningitis

A 
Group B streptococci
Escherichia coli
Staphylococcus aureus
Streptococcus pneumoniae
Neisseria meningitidis
33
Q

SIRS criteria

A 
Temperature
>38oC or <36oC
Heart rate
>90/min
Respiratory
>20/min
PaCO2
<32mmHg (<4.3kPa)
WBC
>12 or <4 x109/L

SIRS 2+ same patient

34
Q

SOFA

A

Sequential organ failure assessment. Sepsis when documented/suspected infection with SOFA 2+ above current baseline

Fi02
Platlets
Billirubin
GCS
Creatine
Urine output
35
Q

QSOFA

A 
Respiratory
>20/min
CNS
Altered mentation
SBP
<100mmHg
36
Q

Septic shock definition

A

Septic shock
Sepsis presenting with MAP <65mmHg (quick identification and primary/community)
Sepsis requiring vasopressors to maintain MAP above 65mmHg plus serum lactate >2mmol/L (inpatient

37
Q

CARS definition

A

Compensatory anti-inflammatory response syndrome (CARS)

A body-wide suppression of immune responses following overwhelming pathogen exposure

38
Q

Sepsis summary

A

Virulent pathogens, compromised defenses - poorly controlled + spreading infections - organ damage + sepsis

Year 2 (12 decks)

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