Nurs 5315: Adv Patho Exam 1
E. Cells decrease in size
P. Still functional; imbalance between protein synthesis and degradation. Essentially
there is an increase in the catabolism of intracellular organelles, reducing structural
components of cell
Physiologic: thymus gland in early childhood
Pathological: disuse (muscle atrophy d/ decrease workload, pressure, use, blood supply,
nutrition, hormonal stimulation, or nervous stimulation) - Atrophy
E: cells increase in number, mitosis (cell division) must occur, size of cell does not
change
Phys: increased rate of division, increase in tissue mass after damage or partial
resection; may be compensatory, hormonal, or pathologic
Patho: abnormal proliferation of normal cells usually caused by increased hormonal
stimulation (endometrial). increase of production of local growth factors
Ex: removal of part of the liver lead to hyperplasia of hepatocytes. uterine or mammary
gland enlargement during pregnancy - Hyperplasia
E. Not true adaptation; Cells abnormal change in size, shape, organization (classified as
mild, moderate, severe)
P. caused by cell injury/irritation, characterized by disordered cell growth. aka atypical
hyperplasia or pre-cancer, a disorderly proliferation
Physiologic: N/A
Pathologic: squamous dysplasia of cervix from HPV shows up on pap smear, breast
cancer development; pap smears often show dysplastic cells of the cervix that must
undergo laser/surgical tx - Dysplasia
E: reversible change, one type of cell changes to another type for survival
P: reversible; results from exposure of the cells to chronic stressors, injury, or irritation;
Cancer can arise from this area, stimulus induces a reprogramming of stem cells under
the influence of cytokines and growth factors
Ex: Patho: Columnar cells change to squamous cells in lungs of smoker or normal
ciliated epithelial cells of the bronchial linings are replaced by stratified squamous
epithelial cells.; Phys: Barrett Esophagus- normal squamous cells change to columnar
epithelial cells in response to reflux, aka intestinal metaplasia - Metaplasia
E. inadequate oxygenation of tissues
P. decrease in mitochondrial function, decreased production of ATP increases anaerobic
metabolism. eventual cell death.
C.M. hypoxia, cyanosis, cognitive impairment, lethargy - Hypoxia injury
E. normal byproduct of ATP production, will overwhelm the mitochondria- exhaust
intracellular antioxidants
P. lipid peroxidation, damage proteins, fragment DNA

C.M. development in Alzheimer's, heart disease, Parkinson's disease, Amyotrophic
Lateral Sclerosis - Free radical and ROS
E. mood altering drug, long term effects on liver and nutritional status
P. metabolized by liver, generates free radicals
C.M. CNS depression, nutrient deficiencies-Mag, Vit B6, thiamine, PO4, inflammation
and fatty infiltration of liver, hepatomegaly, leads to liver failure irreversible - Ethanol
Na and H2O enter cell and cause swelling. Organ increases in weight, becomes
distended and pale. Associated with high fever, hypocalcemia, certain infections -
Oncosis
Liver and germ cell tumors - Alpha Fetoprotein Origin
GI, pancreas, lung, breast tumors - Carcinoembryonic Antigen
prostate tumors - Prostate Specific Antigen
from epithelial tissue- renal cell carcinoma - Carcino-
from connective tissue- chondrosarcoma - Sarco-
preinvasive epithelial malignant tumors of glandular or squamous cells- cervix -
Carcinoma in situ
Multiple organs including brain - Lung ca metastasis
Liver, lungs - Colorectal ca metastasis
Liver, lungs, brain - Testicular ca metastasis
Bones (especially lumbar spine), liver - Prostate ca metastasis
Liver, bones, lymphatics - Head and neck ca metastasis
Peritoneal surfaces, diaphragm, omentum, liver - Ovarian ca metastasis
Lungs - Sarcoma metastasis
In transit lymphatics, lung, liver, brain, GI tract - Melanoma metastasis
Local invasion, followed by invasion of surrounding tissues. Cells then may invade blood
and lymphatic vessels. They must survive in circulation, then enter and survive in a new
location. Then the cells can multiply and form a new tumor. - Mechanisms of ca
metastasis
T= tumor size >/= correlates with metastatic ability

N= whether lymph nodes are involved
M= extra nodal involvement (liver, lungs) - TNM staging system
In venous system- 20% - Intravascular fluid compartment
The measure of solute concentration in a fluid.
280-295 mOsm - Osmolality
Surrounds the cells and bathes them in nutrients- 20% - Interstitial fluid compartment
Within the cells- 40% uk - Intracellular fluid compartment
Passive- the movement of water from an area of low concentration of solute to one of
higher concentration - Osmosis
Pulling- the amount of pressure or force that is exerted by solute molecules of a given
compartment - Osmotic pressure
Blood pressure- pushes fluid outside of the vessels, the force of fluid against the walls of
a compartment- venous obstruction, Na and water retention - Hydrostatic pressure
Colloid pressure keeps water inside the compartment, attracts water from interstitial
space back into the capillary- losses or diminished albumin - Oncotic pressure
The amount of blood within the arterial space- ECF changes will cause changes in the
EABV in the same direction - Effective arterial blood volume
Activated by low blood volume, triggers release of renin which converts angiotensinogen
to angiotensin 1. ACE converts angiotensin 1 to angiotensin which causes arterial
vasoconstriction and stimulates release of aldosterone. Aldosterone stimulates renal Na
reabsorption and K+ excretion. Water is retained, less urine is produced, blood volume
increases. - Renin Angiotensin Aldosterone System
ANP and BNP- released by heart- works opposite RAAS to decrease blood volume,
promotes urinary excretion of Na and water - Natriuretic hormones
Dehydration- intake is not enough for body's needs
C.M. Poor skin turgor, dry mucous membranes, sunken eyes, sunken fontanelles,
decreased urine output, fatigue - Fluid volume deficit
Fluid intake exceeds body's needs
C.M. Edema, rales, HTN, weight gain, bounding pulses, intake> output, JVD,
restlessness or anxiety - Fluid volume excess
Accumulation of fluid within the interstitial space- venous obstruction, Na and water
retention

C.M. can be localized or dependent, tightness of skin, facial swelling, rales, decreased
wound healing, increased risk of pressure sores, weight gain - Edema
K+ enters cell with glucose transport. Monitor Type II DM for hypokalemia - insulin
effect on K+
albuterol, beta blockers, and alpha adrenergic antagonists cause K+ movement into the
cell. Alpha adrenergic receptors shift K+ out of the cell - Adrenergic agents effect on K+
hyperosmolality causes water to shift out of cell via osmosis. K+ will also shift out,
causing hyperkalemia. - Osmolality effect on K+
intracellular K+ is released into bloodstream - Cell lysis effect on K+
cellular ATP is diminished, opening K+ channels and allowing K+ to leave cell - Exercise
effect on K+
excretion and absorption of K+ is regulated by tubule system - Kidneys effect on K+
mag inhibits the potassium channels, keeping balance. when mag is low, more K+ exits
the call, and is excreted via the kidneys. - magnesium and potassium
E. increased acid production, loss of bicarb, diminished renal excretion of hydrogen
C.M hyperventilation (compensatory), h/a, n/v/d, dehydration, hypotension
pH <7.4 HCO3 <22 - metabolic acidosis
E. GI loss, diuretic use
C.M. slow, shallow respirations, irritability, twitching, s/s of hypokalemia
pH >7.4 HCO3 >26 - metabolic alkalosis
E. cns depression, airway abnormalities
C.M. restless, confused, seizures, tachycardia
pH <7.4 PaCO2 >44 - respiratory acidosis
E. usually anxiety, PE, chf, salicylate OD, illegal drugs
C.M. light-headed, confused, tetany
pH >7.4 PaCO2 <38 - respiratory alkalosis
Paired genes on autosomal chromosomes - Allele
Outward appearance of an individual - Phenotype
A map of ones specific genes - Genotype
Two or more alleles which occur with an appreciable frequency in a population -
Polymorphic

Two dominant or recessive alleles - Homozygous
When both a dominant and a recessive allele are present - Heterozygous
Trait seen in phenotype - Dominant
Trait not seen in phenotype - Recessive
first 22 of 23 chromosomes - Autosomal chromosomes
23rd pair of chromosomes - sex-linked chromosomes
E. Increase in cell size
P. Caused by hormonal stimulation or increased functional demand, which increased
the cellular protein in the plasma membrane, endoplasmic reticulum, myofilaments,
and mitochondria (not cellular fluid)
Physiologic: skeletal muscle hypertrophy for persons doing heavy work/weight lifting.
one kidney removed, the other kidney increases in size to accommodate for workload
Pathologic: cardiomegaly from HTN/L ventricular hypertrophy - Hypertrophy
ischemia which progresses to hypoxia.
Intracellular enzymes such as CK, LDH, AST, ALT, troponin - Hypoxic Injury
Clinical Manifestations
decreased O2, loss of H/H, decreased RBC production, disease of heart/lungs, ischemia
- Hypoxic Injury
-most muscle cells, including heart excrete what enzyme - CK enzymes
- muscle cells, liver cells, heart cells, RBCs, brain secrete what enzyme - LDH
- liver cells (s) - AST enzymes are found where?
- liver cells (L enzyme) - ALT enzymes are found where?
- cardiac cells - Troponin enzymes are found where?
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. - Hypoxic Injury Pathophysiology
have unpaired electron in its outer shell, making molecule unstable and highly reactive.
aka being oxidized - Free Radical Etiology

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byproduct of ATP production in the mitochondria - Reactive Oxygen Species ROS
Etiology
to stabilize self, it will steal an electron from another molecule or give up and electron.
The free radical will often steal an electron from another molecule, making that
molecule a free radical - Free Radical and Clinical Manafestations
can overwhelm mitochondria and exhaust intracellular antioxidants, causing cell
injury/disease - Reactive Oxygen Species (ROS) Clinical Manafestations
may by initated with in cells by (1) absorption of extreme energy sources such as
radiation or UV light; (2) the occurrence of endogenous reactions, such as redox
reactions in which oxygen is reduced to water have role in development of Alzheimer's,
Parkinson's, Amyotrophic Lateral Sclerosis. Antioxidants are our bodies' defense,
reducing agents that provide missing electron that can stabilize the ________ - Free
Radical and Pathophysiology
cause lipid peroxidation, damage proteins which maintain ion pumps and cellular
transport, fragment DNA and causes less protein synthesis, cause chromatin
destruction, and damage mitochondria. - Reactive Oxygen Species (ROS)
Pathophysiology
ETOH is metabolized to acetaldehyde in the cytoplasm of the cell, enzyme alcohol
dehydrogenase (ADH) helps with conversion - Ethanol Etiology
adverse effects on liver and causes nutritional disorders. acute effects in the liver include
inflammation, fatty infiltration, hepatomegaly, acute liver necrosis and suppressed fatty
acid oxidation. liver failure is irreversible effect of chronic abuse - Ethanol Clinical
Manafestations
Conversion oxidized niacin (NAD+) is reduced to NADH. In the mitochondrial
acetaldehyde is further converted by ADH to acetate and further oxidized niacin (NAD+)
is reduced to NADH. the increased NADH/NAD+ ratio in the liver causes the following
1.Pyruvate change to lactic acid causing lactic acidosis
2. Oxaloacetate converted to malate, preventing gluconeogenesis leading to fasting
hypoglycemia
3. Glyceraldehyde to glycerol which combines with fatty acids and forms triglycerides,
leads to triglycerides in the liver, aka hepatosteatosis
4. decreases citric acid cycle production of NADH which leads to utilization of Acetyl-
CoA for ketogenesis (causing ketoacidosis) and lipogenesis (causing hepatosteatosis) -
Ethanol Pathophysiolody
cellular swelling, cellular injury because with most injuries there is some amount of O2
deprivation causing hypoxic injury - Oncosis Effects and Clinical Implications
spectrum of cell changes after the cell dies - Necrosis

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necrosis which results from sudden insufficiency of arterial blood flow - Infarct
liver cell, ketogenesis occurs in the mitochondria of the hepatocyte
result of unavailability of glucose - Role of the hepatocytes
Ketogenesis is the formation of ketone bodies and occurs mostly in the mitochondria of
the hepatocytes (liver cells) - Role of the mitochondria
lack of glucose
-occur from the depletion of carbohydrate stores or may occur bc the cell is not able to
use glucose but the individual is hyperglycemic (type 2 DM) - Triggers for ketogenesis
processed by hepatocytes and undergoes transformation to 3 ketone bodies:
Acetoacetate, Acetone and B-hydroxybutyrate (basis of ketoacidosis)
-States of starvation or uncontrolled DM, cells do not receive enough glucose to produce
energy, resulting in acceleration of the B-oxidation cycle and increasing oxidation of
fatty acids or energy. B-oxidation cycle results in formation of acetyl-CoA - Role of
Acetyl-CoA
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 - Effect on oxaloacetate
Liver and germ cell tumors - Alpha Fetoprotein (AFP)
GI, pancreas, lung, breast, ect tumors - Carcinoembryonic Antigen CEA
Germ cell tumors - Beta Human Chorionic gonadotropin B-hCG origin
Prostate tumors - Prostate Specific Antigen PSA
arise from epithelial tissue - Carcino- (prefix)
connective tissue (muscle and bone tissue)
malignant cancers of the skeletal muscle are known as rhabdomyosarcomas - Sarco-
(prefix)
arise from ductal or glandular structures - adeno (prefix)
-preinvasive epithelial malignant tumors of glandular or squamous cell origin
-# 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 - Carcinoma in Situ
originates from precursor cells or blasts (immature or embryonic tissue).
Ex: children, neuroblastoma, retinoblastoma - -blastoma (suffix)

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NURS5315 Pathophysiology Practice Exam With Answers (186 Solved Questions)

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