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ADVANCED PATHO-ALTERED CELLULAR FUNCTION AND CANCER STUDY GUIDE QUESTIONS AND ANSWERS

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ADVANCED PATHO-ALTERED CELLULAR FUNCTION AND CANCER STUDY GUIDE QUESTIONS AND ANSWERS

Institution
NURS 5315 Advanced Pathophysiology
Course
NURS 5315 Advanced Pathophysiology

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54 Multiple choice questions

Definition 1 of 54
Etiology: over accumulation or under secretion of uric acid Clinical Manifestations:Use of
diuretics bc they trigger kidneys to increase the absorption of uric acid. The liver may produce
more uric acid if a diet high in red meat, cream sauces, or red wines bc they are high in purines.
Pathophysiology:Increase in purine degradation which leads to increased amounts of uric acid.
Uric acid is a byproduct of purine degradation, accumulation of uric acid not excreted by the
kidneys lead to increased uric acid in the kidney, heart, earlobes and joints. Inflammation
process is triggered and the right great toe is most commonly affected, but it can affect any
joint.

Hypoxic Injury

Rhabdomyolysis

Atrophy


Gout

Definition 2 of 54
Definition:connective tissue Ex:malignant cancers of the skeletal muscle are known as
rhabdomyosarcomas

-oma (suffix)


-blastoma (suffix)


Sarco- (prefix)

Head and Neck

,Definition 3 of 54
bones (especially lumbar spine), liver - regional lymph and veins which drain to batson plexus

Colorectal


Ovarian

Prostate


Testicular

Definition 4 of 54
E: cells abnormal changes in shape, size, organization P: caused by cell injury/irritation,
characterized by disordered cell growth. aka atypical hyperplasia or pre-cancer Ex:pap smears
often show dysplastic cells of the cervix that must undergo laser/surgical tx

Hypertrophy


Gangrenous Necrosis

Dysplasia

Hyperplasia

Definition 5 of 54
Definition:-preinvasive epithelial malignant tumors of glandular or squamous cell origin-
localized to the epithelium- not yet malignant- 3 fates: can remain stable for long time,
progress to invasive/met CA, or regress and disappear Ex:- # of sites including cervix, skin, oral
cavity, esophagus and bronchus- in breast, ductal carcinoma in situ (DCIS) fills the mammary
ducts but has not progressed to local tissue invasion

Role of Acetyl-CoA


-blastoma (suffix)

Urate accumulation

Carcinoma in Situ

,Definition 6 of 54
Etiology:decreased O2,loss of Hgb or Hgb function, decreased RBC production, disease of
heart/lungs, ischemia Clinical Manifestations: ischemia which progresses to hypoxia.
Intracellular enzymes as follows: CK-most muscle cells, including heart,LDH- muscle cells, liver
cells, heart cells, RBCs, brain,AST- liver cells,ALT- liver cells Troponin- cardiac cells Patho: lack
of O2 causes decrease in mitochondrial function, causing decrease ATP production and
increases anaerobic metabolism (generating ATP from glycogen), eventually anaerobic
metabolism will stop and the cell will die. Reduction of ATP impairs Na/K pump, leads to
increased Na/Ca in cell, K is diffused out of cell, water diffuses into cell causing swelling,
ribosomal dilation and malfunction occur. Ribosomes produces protein and when it
malfunctions causes decrease in protein synthesis. Death will occur if injury is not stopped.

Rhabdomyolysis


Hyperplasia

Free Radical and Reactive Oxygen Species (ROS)

Hypoxic Injury

Definition 7 of 54
lungs- IVC, RV, PA

Breast

Prostate


Melanoma

Sarcoma

, Definition 8 of 54
Role:Oxaloacetate is also used in gluconeogenesis, during starvation & uncontrolled DM
oxaloacetate levels are insufficient due to gluconeogenesis... this depletion furthers the
amount of acetyl-CoA which activates ketogenesis Clinical Implications:Oxaloacetate (an
intermediate) is involved in: Citric acid cyclegluconeogenesisurea cycleamino acid
synthesisfatty acid synthesis

Role of the mitochondria

Role of the hepatocytes

Role of Acetyl-CoA

Effect on oxaloacetate

Definition 9 of 54
Alcohol is metabolized by alcohol dehydrogenase (ADH) into acetaldehyde, then further
metabolized by aldehyde dehydrogenase (ALDH) into acetic acid, which is finally oxidized into
carbon dioxide (CO2) and water ( H2O).[6] This process generates NADH, and increases the
NADH/NAD+ ratio. A higher NADH concentration induces fatty acid synthesis while a
decreased NAD level results in decreased fatty acid oxidation. Subsequently, the higher levels
of fatty acids signal the liver cells to compound it to glycerol to form triglycerides. These
triglycerides accumulate, resulting in fatty liver.

Cancer cell metastasis usually involves the following steps:

Free Radical and Reactive Oxygen Species (ROS)

Effect on oxaloacetate

Hepatocellular damage:Fatty Liver

Definition 10 of 54
peritoneal surfaces, diaphragm, omentum, liver- direct extension, peritoneal seeding,
mesenteric veins

Sarco- (prefix)


Melanoma

Infarct

Ovarian

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Institution
NURS 5315 Advanced Pathophysiology
Course
NURS 5315 Advanced Pathophysiology

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Uploaded on
September 24, 2024
Number of pages
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Written in
2024/2025
Type
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