Final part 3

Question 1

What are protoncogogenes 4

Answer 1

Genes that regulate cell growth but can become unlocked from carcinogens or oncogenetic viruses
once they become unlocked they work like oncogenes-tumor inducing
this means the ability and properties that the cell had in fetal development are now active
it is immature, dedifferentiated, change from normal to make
and can make new proteins

Question 2

Oncogene proteins
are located?
2 ex
and one more thing they produce

Answer 2

Located on the cell membrane
in blood tests
CEA and Fetalprot
produce hormones

Question 3

What are tumor decreasing genes
What happens to them during cancer
Two examples and about them

Answer 3

They regulate growth by not letting cells go through the cell cycle
Are mutated or turned off
BRAC1 and BRAC 2 have inherited mutations for breast and cervical cancer

Question 4

What is ACP gene

Answer 4

Tumor suppressor gene that can have a Family mutation gene for adenomatous
polyposis- colorectal cancer

Question 5

Model of development of cancer

Answer 5

Initiation- Inherited or acquired
Promotion- Reversible proliferation
Progression-possible metastasis tumor growth

Question 6

Initiation
What is it?
What about inherited?
What about acquired- 3 examples

Answer 6

Any change or mutation in usual DNA sequencing
if inherited -sm risk but high risk
carcinogens- Alkylating drugs or immunosuppressants can cause secondary leukemia that is resistant to chemo
Radiation- Atomic bomb and UV
Viral- Epstein barr, HIV, Hep B, HPV

Question 7

CEP

FP

Answer 7

Carcenoembryonic antigen is a tumor cell protein

Alpha fetoprotein

Question 8

What are the oncofetal antigens and how do we use them what are they 2

Answer 8

Tumor antigens from cell in the fetal state
use them as tumor markers
CEA and AFP

Question 9

Thrombocytopenia numbers

Answer 9

tcp-150,000
bleed risk prolonged- 50,000
spontaneous bleed 20,000

Question 10

What is polycythemia?

Two types and about them

Answer 10

The production on presence of increased numbers of RBC
Primary (vera) or secondary
P- chronic-all BC involved=viscosity and volume= meglys and clotting
S-hypoxia driven or independent
driven-Hypoxia stimulates EPO
S-independent- tumor is making EPO
There is no splenomeg with secondary

Question 11

S/S of primary polycythemia

Answer 11

HA, vertigo, tinnitus, visual changes
pruitus, paresthesia, erythromelagia-buring and red of hands and feet
angina, HF, intermittent claudication, clot issues hypoxia and stroke
Hyperuricemia, hemorrhage, ulcers, meylofibrosis, leukemia,

Question 12

One lab difference between primary and secondary poly

Tx

Answer 12

Primary-Low to normal EPO
secondary- high
Phlebotomy to normalize Hematocrit

Question 13

Types of pneumo

Answer 13

● Spontaneous- Rupture of bleb – Primary (idiopathic) & Secondary (to lung disease→COPD)
● Iatrogenic - Caused by medical procedures
● Traumatic penetrating (open)
● Traumatic blunt (closed)
● Hemothorax
o Blood in pleural space
o Treat with chest tube
● Hemopneumothorax
● Chylothorax
o Lymphatic fluid in pleural space
o Treat conservatively, with meds, surgery, or pleurodesis.
● Tension Pneumothorax - medical emergency
o Accumulation of air in pleural space that does not escape
o Causes mediastinal shift and hemodynamic instability.
o Can occur with penetrating (open) or blunt (closed) pneumothorax.
o tracheal deviation!
● S/S of pneumothorax
o dyspnea
o anxiety
o tachycardia
o pleural pain
o asymmetrical chest wall expansion
o diminished breath sounds

Question 14

thorancentesis

Answer 14

● Used to obtain specimen of pleural fluid for dx, removal, or giving meds
● complications = Hypoxia, pneumothorax
● Don’t remove fluid too quickly = hypotension, hypoxemia, reexpansion, pulm. edema, spasms?
● X-ray after to check for pneumothorax

Question 15

Tumor Lysis Syndrome

Answer 15

● Hyperuricemia
● Hyperphosphatemia
● Hyperkalemia
● hypocalcemia. p262 table 15.19
● Occurs 24-48 hrs after starting chemo. May last 5-7 days. Can lead to acute kidney injury (↑BUN & Cr)
● Patient safety: monitor f/e and cardiac function. Anything else?

Question 16

HITT

Answer 16

● platelets reduced by 50% (below 150,000)
● 5-10 days after trt.
● DVT, PE, venous thrombosis (the m/c problem), arterial vascular infarcts - leads to stroke, kidney damage
● Platelet destruction and vascular endothelial injury are the 2 major responses to an immune-mediated response to heparin
● Antibodies are created against the PF4-platelet-heparin complex which are removed prematurely from circulation, leading to thrombocytopenia and platelet-fibrin thrombi
● this is basically like having an allergy to heparin; the patient should NOT take heparin, ever

Question 17

labs

Answer 17

Question 18

TACO

Answer 18

● Fluid given faster than circulation can handle; blood products are hypertonic
● Cough, dyspnea, pulmonary congestion, headache, hypertension, tachycardia, distended neck veins
● Patient HOB raised, diuretics, oxygen
● May be able to continue the transfusion depending on situation

Question 19

Acute Hemolytic

Answer 19

● ABO incompatibility
● Antibodies in patient’s plasma attach to antigens on transfused RBCs causing lysis of cells
● Symptoms usually occur quickly after blood started: Chills, fever, low back pain, hemoglobinuria, flushing, tachycardia, tachypnea, hypotension, jaundice, acute renal failure
● Stop the blood but keep IV patent. Treat shock, draw blood for testing, insert Foley, renal dialysis

Question 20

Transfusion Related Acute Lung Injury (TRALI)

Answer 20

● Occurs when donor plasma contains WBC antibodies. Causes fluid leak into lungs Þ pulmonary edema
● Dyspnea, hypotension, and fever usually begin 1-2 hours after the transfusion, but possibly up to 6 hrs later; can have pulmonary edema and acute resp distress
● Ventilatory support may be needed for several days

Question 21

Febrile Non-hemolytic

Answer 21

● Sensitization to donor WBCs, platelets, or plasma proteins
● Most common transfusion reaction
● Sudden chills and fever, headache, flushing, anxiety, muscle pain
● stop the infusion!
● Give antipyretics

Question 22

how do we treat right away for DKA?

Answer 22

O2, then IV- 0.45-0.9 NS, add dextrose if below 250-SLOWWW, short acting insulin, and k+ because of insulin at 0.1 units and increased output, possibly bicarb, Cardiac monitor, labs

Question 23

What is hyperosmolar hyperglycemia

Answer 23

Its an emergency with 600+ BG levels, and severe osmotic diuresis caused by infection or newly diagnosed DM11

Question 24

What are we concerned about hypersomolar hyperglycemia

What can that lead to

Answer 24

Hypovolemia, Hypoelectrolytes, dehydration, Hemoconcentraition, renal perfussion, tissue anoxia (Lactic levels increased)
Seizure, shock, coma, death

Question 25

S/s of hyperos hypergly

Answer 25

Hypovolemia s/s, dehydration s/s, shock s/s, high urine output to low urine output, seizure, high bg, stroke- similarities. LOV issues, s/s of hypoglycemia- mimic alcohol.