Final part 3 Flashcards
What are protoncogogenes 4
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
Oncogene proteins
are located?
2 ex
and one more thing they produce
Located on the cell membrane
in blood tests
CEA and Fetalprot
produce hormones
What are tumor decreasing genes
What happens to them during cancer
Two examples and about them
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
What is ACP gene
Tumor suppressor gene that can have a Family mutation gene for adenomatous
polyposis- colorectal cancer
Model of development of cancer
Initiation- Inherited or acquired
Promotion- Reversible proliferation
Progression-possible metastasis tumor growth
Initiation
What is it?
What about inherited?
What about acquired- 3 examples
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
CEP
FP
Carcenoembryonic antigen is a tumor cell protein
Alpha fetoprotein
What are the oncofetal antigens and how do we use them what are they 2
Tumor antigens from cell in the fetal state
use them as tumor markers
CEA and AFP
Thrombocytopenia numbers
tcp-150,000
bleed risk prolonged- 50,000
spontaneous bleed 20,000
What is polycythemia?
Two types and about them
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
S/S of primary polycythemia
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,
One lab difference between primary and secondary poly
Tx
Primary-Low to normal EPO
secondary- high
Phlebotomy to normalize Hematocrit
Types of pneumo
● 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
thorancentesis
● 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
Tumor Lysis Syndrome
● 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?
HITT
● 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
labs
TACO
● 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
Acute Hemolytic
● 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
Transfusion Related Acute Lung Injury (TRALI)
● 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
Febrile Non-hemolytic
● 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
how do we treat right away for DKA?
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
What is hyperosmolar hyperglycemia
Its an emergency with 600+ BG levels, and severe osmotic diuresis caused by infection or newly diagnosed DM11
What are we concerned about hypersomolar hyperglycemia
What can that lead to
Hypovolemia, Hypoelectrolytes, dehydration, Hemoconcentraition, renal perfussion, tissue anoxia (Lactic levels increased)
Seizure, shock, coma, death
S/s of hyperos hypergly
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.
