Pathophysiology NRSG 2312

Exam One Review Modules 1 through 4

September 28, 2017
Professor Joanne Dupuis
Professor Deborah Blackwell
Professor Peter Gunther, MD
 Cellular Biology and
Alterations in Cellular Physiology
Module 1
 Cellular components: What are the functions?
Nucleus DNA and genetic information
Ribosomes involve in protein synthesis
Endoplasmic Reticulum interconnected structures of
cisternae that allow cell to transport protein to Golgi
Golgi Complex packaging proteins
Mitochondria ATP production (power house) give
cells energy to do biological funxtion
 Plasma Cell Membrane (Important)
Phospholipid Bilayer made out of Cholesterol, Proteins
Cholesterol = impt for cell fx
Protein = important for basic cell structure
Selective Permeability Asymetry
Asymmetry: for enzymes like Flipase, Flopase, Apotosis
Changes the shape of the cell or mark cell for cell death
Fluid Mosaic Modes
Functions of Phospholipids, Cholesterol (adhesion construction),
Proteins (enzymatic fx)
(Cholesterol maintain the structure of the membrane and Protein
impt for transporting enzymatic of cell adhesion)
 Cellular Metabolism (dont spend a lot of time)
Digestion
Glycolysis glucose from liver
Citric Acid Cycle: pyruvate to Acetyl CoA, ADP -ATP
Oxidative Phosphorylation
ADP to ATP production, glucose from liver
 Cellular Adaption (Important slide)
Atrophy shrinking of the cells cell get a smaller. Leg in a cast for a
period of time.
Hypertrophy larger cells, body builder, they dont make more cell,
they make bigger cell, L AV Hypertrophy heart
Hyperplasia More cells but same size. Benign Prostate get larger in
older man urinary infection
Dysplasia More cells, but the organization of the cells is disrupted
and organized. (preggo) early changes in the cervix cause dysplasia
marked abnormality and inflammation, must be followed closely.
Metaplasia changing of the cell type. Vomiting esophagus
exposed to acid, normal cells will change to different type.
 Cell Injury
Inability to Maintain Homeostasis (internal and
external environment of the cell)
Mechanisms
Cell Death: Apoptosis(Programmed cell death-
GOOD), Necrosis (unplanned cell die, MI heart cell
muscles die with no O2 or blood-BAD), Somatic
Acid Base Pathophysiology
& Fluid and Electrolytes
Module 2 review
 Strong Acid (easily dissociate in water, HCL)/Weak Acid
Bronsted-Lowry Theory : dissociation in water
There are strong acid and weak basic
Volatile (only 1 Carbonic acid) and non Volatile Acids
Volatile means it can be converted into CO2 and water
pH logarithmic scale 1/log of H concentration
Higher pH more alkaline less H+
Lower pH more acid more H+ ions
Homeostasis acid and base balanced
 Buffers: resist large changes in pH maintaining
homeostasis
Buffers: Increased pH :release H+
Decrease pH: bind OH-
H2CO3 HCO3- + H+ H2O + CO2

Respiratory alkosis using up O2

Sedative
 Buffers: (resist changes in pH)
H2CO3 (in the kidney greatest )
RBC contain Carbonic Anhydrase
Blood = Bicarbonate HCO3-
Lungs = CO2 and respiration (greatest buffering
acid)
Proteins: Histidines
 Kidney: Carbonic Anhydrase
Regulate H+ Excretion
Reabsorption of HCO3 key component
Excretion of H+ - key component
Couple H+ with Urinary Buffer NH3
 Metabolic Acidosis something in the system,
increasing of H+ or unable to secrete H+ (renal
failure)
Metabolic Alkalosis getting rid of H+ (nauseous
and vomiting)
Respiratory Acidosis
Respiratory Alkalosis equation to the right,
blowing off O2
 Fluids and Electrolytes
ICF and ECF, there a plasma membrane separating the two, Na+
(external) and K+ (inside)
Inside Blood Pressure (2 pressure):
Hydrostatic Pressure fluid inside the vessels put a force onto it to have fluid
go cross the vessel to ECF.
i.e L Ventricular failure, fluids build up on the right side of the heart causing an increase
of Hydrostatic pressure on the venous side forcing the fluid out of the vessels EDEMA
Oncotic Pressure force that causes fluid to stay inside the vessels, because of
protein (most albumin) force fluid to stay inside, equilibrium solid and liquid
between ICF and ECF.
Albumin with renal failure, cant make of albumin, fluid in belly or leg or peripheral
edema
Balance of the two: Starling Forces : Filtration
 Edema
Fluid into the Interstitial Space(in cell or
outside of blood vessels)
Decreased Plasma Oncotic Pressure (i.e. liver failure)
Increased Capillary Hydrostatic Pressure (i.e. L ven.
failured
Increased Capillary Permeability (due to some type of
inflammation or infection)
Lymphatic Channel Obstruction decrease the
ability to reabsorb fluid
 Water (major fluid in the body)
Aquaporin's channels in plasma membrane and kidney
allow water to be secreted.
Diabetes insipidus where there is a lack of this channel and there
is an unusually amount of water excretion in the urine
Sodium ECF
Potassium ICF
Proteins oncotic pressure
ADH (hormone in kidney, reabsorption of Na and fluid):
Too much Na and too much fluid - tumors
Osmoreceptors, Baroreceptors
 RAAS (renin system - important system -
hypertension) Occurs when there is low BP
JG Cells of KIDNEY produces renin
Renin
Angiotensin 1 (ACE enzyme) in lung
Angiotensin 2
Go to kidney to cause hold on to water, go to lung
vasodilator.
Secrete Aldosterone
Immunity and Inflammation & Infection and
Inflammatory Disorders

Module 3
 Innate Immunity (non-specific barriers to
infection)
Role of Physical Barriers: Skin, Mucous Membranes
Identification of Antigen
Activation of Complement
Recruitment of Inflammatory Mediators
Activation of the Adaptive Immune Response
 Biochemical Barriers
Normal Flora (guts and respiratory mucosa
Antimicrobial Peptides: Defensins, Cathelicidins
Very non-specific, they try to defend against any
invasion of viruses and bacteria
Pattern Recognition opsination by tagging
antigens in a non-specific way and mark them for
phagocytosis
 Inflammation non specific way to fight
infection
Vasodilation veins dilate to slow down circulation so
there will be
Increased Permeability of capillaries
Activation of WBC and Inflammatory Modulators
Warm, red, pain , swelling
Bee sting
 Complement (non-specific)
Opsonization pattern recognition
Chemotaxis ability that complement to stimulate
other inflammatory cells to come into the area
Cell Lysis MAC impt concept to remember
 Adaptive Immunity: Inducible, Specific, Memory
Antigens: Allergens, Haptens, Tumor, Infection(large one)
Antibody: IgA (respiratory epithelium, first line of defense against
antigen infection),
IgG (After M cause its smaller and produces memories), IgM (first guy
out of the B cell because its big)
When newborn is born, the maternal blood is mixed with baby blood IgM is
produced when theres a different in Rh. IgG then produce in the subsequent
pregnancy if the child is Rh+, antibody against it.
IgE (hypersensitivity & parasitic infection), IgD (modulator of T cell fx)
Lymphocytes T-Cells Immune modulation
B-Cells produce Ig (antigen specific)
 Bacterial: Gram Positive, Gram Negative (based on the
cell membrane)
Can reproduce on its on
Viruses: Host cell dependent (respiratory epithelium),
duplicate and replicate inside the hosts cell, and
disrupt host cell and viruses get released
Yeast
Parasites IgE elevation
 Phagocytes
Neutrophils First fighter to fight infections
Mr. Smith goes to the ER, with a cough and a fever.
WBC 16000, predominant of neutrophils bacteria pneumonia
Monocytes Viral infection and becomes
macrophages
Eosinophils hypersensitivity and Parasitic infection
 Hematology
Module 4 review
 Hematologic Pathology
Identify the different cells of the
hematological system and their roles
Describe the role of the different proteins
(ALBUMIN) of the hematological system
Differentiate among the 3 major anemias
Discuss the pathophysiology of polycythemia
vera
Discuss the pathophysiology of porphyria
Hematologic Pathology
Identify the different cells of the hematological system and
their roles
RBC: carries O2, release NO (vasodilator), Biconcave shape to
increase surface area allowing better O2 and CO2 diffusion
Platelets: disc shaped fragments, clot formation, ADP to
produce energy, produce Thromboxane (vasoconstrictor) and
serotonin
Lymphocytes: Granulocytes, T cells (T helper)-immune
modulators, B cells Immunoglobulin producers
Monocytes macrophages (garbage can of the cellular system)
 Hematologic Pathology
Describe the role of the different proteins of
the hematological system
Albumin (largest protein maintain oncotic
pressure)
Globulins: Alpha, Beta, Gamma
 Hematologic Pathology
Differentiate among the 3 major anemias
Macrocytic-Normochromic
Primary cause is B12 (from green vegetable cant go through the gastric)
deficiency
(gastric bypass B12 from greens diet cannot go through the gastric mucosa to small
valve to absorbed. intrinsic factor reduction of B12, large cells anemia large RBCs -
MACROCYTIC),
Microcytic-Hypochromic
RBCs are small
Iron deficiency, SA , Red blood in rectum pneumonic for Iron defiency.
Normocytic-Normochromic
Aplastic, anemia chronic disease inflammatory process (arthritis, Renal
failure), hemorrhage, SS, hemolytic
 Hematologic Pathology
Discuss the pathophysiology of Polycythemia Vera
Overproduction RBCs primary or secondary (secondary
causes by hypoxia or elevation in altitude with low O2
retention)
High Hemoglobin and hemacrit, & cause thickening of the blood
(necrosis problem with Heart disease.
Clinical and Lab findings
Treatment phlebotomy to reduce the amount of blood
and underlying causes
 Hematologic Pathology
Discuss the pathophysiology of Porphyria
(hemoglobin synthesis defect in taking
porforin and making them into hemoglobin)
Increase in Porforin causes abdominal pain,
depression, light sensitivity.
Discuss the pathophysiology of Hemochromatosis
Diagnosis and treatment increase amount of RBCs,
increase of iron, stuck in the liver tx phlebotomy
 Hematologic Pathology
Thrombocytopenia low platelets count (heparin-
induced, when patient has been in the hospital for
a long time)
Hodgkins Lymphoma.. Reed Sternberg Cells
Non Hodgkins Lymphoma
AML, CML, ALL, CLL (not too concerned about)
 Oncology
The biology
The epidemiology certain cancer exposure, smoking lung cancer. Strong hereditary form
breast and colon cancer
The staging *** insight to invasion, important in define the therapy
Stage 1 or 2 surgery or radiation makes sense
Stage 3 or 4 no surgery or radiation --> systemic therapy.
The clinical presentation weight loss, anorexia, multitude of system. Paraneoplastic
syndromes Lymphedema Fever.
The treatment options - surgery, chemo, radiation newer therapy
Stimulate their own immune system to take out the cancer cells.
Cancer make it own blood supply to keep it alive (can use non-chemotherapy to provide tx for
cancer)
Cancer or paraneoplastic (other symptoms that are unrelated to the cancer Lung cancer
produce ADHD like substances kidney reabsorption of Na and water.
QUESTIONS????
Study Hard
Do Well!