Unit 4

Question 1

Taste receptor for umami

Answer 1

T1R1 T1R3

l-glutamate

Question 2

Taste receptor for sweet

Answer 2

T1R2 T1R3

sugars, glycine + d amino acids

Question 3

Taste receptor for bitter

Answer 3

30 T2R

Cycloheximide

Question 4

Taste receptor for sodium

Answer 4

ENaC

NaCl

Question 5

Taste receptor for sour

Answer 5

PKd2L1 acids

CA IV
carbonated drinks

Question 6

Routes malignancy

Answer 6

Blood
lymphatics
local
transcoelomic - peritoneal cavity

Question 7

HER 2

Answer 7

ONCA-GENE

Question 8

BRACA 1/2

Answer 8

TSG

Question 9

Innervation tongue paillae

Answer 9

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

Question 10

Describe how viruses cause cancer?

Answer 10

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.

Question 11

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

Answer 11

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.

Question 12

How ALV became viral oncagene

Answer 12

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.

Question 13

why not all cells infected ALV become tumours

Answer 13

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.

Question 14

How lesion V3 affects ear

Answer 14

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

Question 15

joints name ossicles

Answer 15

synovial

Question 16

Joint name stapies

Answer 16

ball + socket

Question 17

Innervation stapedius

Answer 17

facial nerve

Question 18

Innervation tensor tympnai

Answer 18

V3 division trigeminal

Question 19

Visual pathway

Answer 19

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

Question 20

Why not all cells infected ALV form tumours

Answer 20

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.

Question 21

How HPV 16 /18 creates tumour

Answer 21

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.

Question 22

how cells get immortality

Answer 22

express telomerase reverse transcriptase (hTERT)

Question 23

6 step metastasis

Answer 23

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

Question 24

Neoplasm: .

Answer 24

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

Question 25

Dev invasive carcinoma

Answer 25

* 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.

Question 26

SIRS to sepsis

Answer 26

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

Question 27

CARS

Answer 27

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

Question 28

Sepsis organisms

Answer 28

Eschericia coli | Staph aureus

Question 29

Sepsis 6

Answer 29

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 ```

Question 30

Sepsis from SIRS

Answer 30

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

Question 31

Septic shock

Answer 31

Increase TF - hypercogulation - depletion clotting factors - increased anticogulation -> low BP/ MAP. SIRS - Increase TNF alpha, Oedema + hypoperfusion - low BP/MAP

Question 32

Pathogens meningitis

Answer 32

``` Group B streptococci Escherichia coli Staphylococcus aureus Streptococcus pneumoniae Neisseria meningitidis ```

Question 33

SIRS criteria

Answer 33

``` 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

Question 34

SOFA

Answer 34

Sequential organ failure assessment. Sepsis when documented/suspected infection with SOFA 2+ above current baseline ``` Fi02 Platlets Billirubin GCS Creatine Urine output ```

Question 35

QSOFA

Answer 35

``` Respiratory >20/min CNS Altered mentation SBP <100mmHg ```

Question 36

Septic shock definition

Answer 36

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

Question 37

CARS definition

Answer 37

Compensatory anti-inflammatory response syndrome (CARS) | A body-wide suppression of immune responses following overwhelming pathogen exposure

Question 38

Sepsis summary

Answer 38

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