NUR 2063 Pathophysiology Final Exam Study Guide Modules 1-10

Pathophysiology Final Exam Study Guide

Modules 1-10

Module 1

Chapter 2

I.        General Adaptation Syndrome and Allostasis

a.  Alarm Stage: Fight-or-Flight response due to stressful stimuli.

b.  Resistance Stage: Nervous & Endocrine systems returning the body to homeostasis

c.  Exhaustion Stage: Point where bofy can no longer return to homeostasis

Chapter 24

Revise NCLEX RN Exam

II.       Body Fluid Homeostasis: Pertains to water within the body and the particles dissolved in it.

i.  Fluid Distribution: Occurs through osmosis, water moves to higher osmolality, cell membranes permeable to water, not elec- trolytes.

ii. Extracellular Fluid: OUTSIDE THE CELL

1.  1/3 BODY FLUID IN ADULTS

2.  Infants have more extracellular fluid as compared to intracel- lular

iii. Intracellular Fluid: INSIDE THE CELL

1.  2/3 BODY FLUID IN ADULTS

III.      Fluid Imbalances a.  Volume Deficit

i.  Etiology: Caused by removal of a sodium-containing fluid from the body

ii. Clinical Manifestations:Sudden weight loss, postural blood pres- sure decrease with concurrent increased heart rate, flat neck veins, lightheadedness, dizziness, syncope, oliguria, decreased skin tur- got, dryness of oral mucus membranes, hard stools, soft sunken eyeballs, lonitudinal furrows in the tongue

1. INFANTS: fontanel may be sunken, neck veins are not reli- ably assessed in infants

b.  Volume Excess

i.  Etiology: Amount of extracellular fluid is abnormally increased, vascular and intersitial areas have too much fluid

ii. Clinical Manifestations:

1. Circulatory Overload: Bounding pulse, neck vein distention in upright position, crackles in dependent portions of lungs, dyspnea, orthopnea

2. Sudden Weight Gain: A sensitive measure of extracellular fluid

3. INFANT: Bulging fontanel, assessment of neck veins is not effective in infants

4. Edema

5. ADVANCED: Frothy sputum of pulmonary edema

IV.      Body Fluid Concentration

a.  Hyponatremia: Serum Sodium conentration below the lower limit of nor- mal

i.  Clinical Manifestations:

1. Mild Central Nervous System Dysfunction: Malaise, anorexia, nausea, vommiting, headache

2. Severe Central Nervous System Dysfunction: Confusion, lethargy, seizures, coma, fatal cerebral herniation

b.  Hypernatremia: Serum sodium concentration above upper limit of normal

i.  Etiology/Causes: Gain of more salt than water, loss of more water than salt

c.  Interstitial Fluid Volume i.  Edema:

V.       Electrolyte Imbalances a.  Serum Potassium

i.  Hypokalemia: decreased potassium ion concentration in extracel- lular fluid

1.  Etiology:

a.  Decreased Intake: Usually in conditions that cause a decreased oral intake

b.  Shift into the cell from extracellular fluid

c.  Increased Excretion: Renal, through feces, Sweat, GI Tract (Emesis, diarrhea) Diuretics

ii. Hyperkalemia: Rise of serum potassium levels above 5 MEQ/L

1.  Clinical Manifestations:

a.  Early, Mild: Intesional Cramping, Diarrhea

b.  Late, More severe: Musclue weakness: (Ascending, beginning in lower extremities) Cardiac Dysrhythmias, even cardiac arrest

b.  Serum Calcium

i.  Clinical manifestations:

1. HYPO-

a. Clinical Manifestations:

i.  Hyperexcitability of Neuromuscular cells: possitive trousseau sign, positive chvostek sign (not reliable in infants), parethesias, muscle twitching and cramping, hyperactive reflexes, carpal spasm, pedal spasm, tetany, laryn- gospasm, seizures, cardiac dyshythmias

2. HYPER-

Module 2

Chapter 8

a. Clinical Manifestations: decreased neuromuscular excitability, muscle weakness, diminished reflexes, cardiac dysrhythmias, anorexia, nausea, emesis, fa- tigue, polyuria, constipation, headache, confusion, lethargy, personality change, renal calculi, pathologic fractures

I.        Transmission of Infection

a.  Chain of Transmission:

Chapter 9

I.        Innate Defenses and Inflammation a.  Inflammation

i.  Neutrolize and destroy invading and harmful agents ii. limit spread of harmful agents to other tissue

iii. prepare damaged tissue for repair

iv. Redness, swelling, heat, pain, loss of function

b.  Histamine: Most important mediatior

i.  Causes: Increased vascular permeability, vasodilation, urticaria, smooth muscle constriction, increased mucus secretion, pruritis

ii. Clinical Manifestations:

1.  Mild: Hives, seasonal alergic rhinitis, eczema

2.  More problematic symptoms: throat constriction, localized edema, wheezing, tachycardia

3.  Anaphylaxis: Most life-threatening reaction; occurs in very small number of highly allergic individuals

iii. Treatment:

1.  Antihistamines: block effects of histamine

2.  Beta-Adrenergics: decrease bronchoconstriction

3.  Corticosteroids: decrease inflammatory response

4.  Anticholinergics: Block parasympathetic system

5.  IgE therapy: Inhibits binding of IgE to mast cells

6.  Epinephrine: Adrenergic agent given subQ or IV during acute allergic reactions

c.  Systemic Manifestations of Inflammation

II.       Passive Immunity: Provided when a person is given antibodies to a disease rather than producing them on their own. (from mother/ artificial)

III.      Active Immunity: Production of antibodies by the immune system in re- sponse to the presence of an antigen (Vaccines/Illness)

Chapter 10

I.        Excessive Immune Responses

a.  Autoimmunity: Immune system attacks own tissues

b.  Hypersensitivity: Normal immune response that it inapropritately trig- gered, excessive, produces undesireable effects on the body

i.  Type I Sensitivity (Immediate Hypersensitivity)

1. Reation occurs 15 to 30 minutes after exposire to antigen/al- lergen

2. Clinical Manifestations:

a. Mild: Hived, seasonal allergic rhinitis, eczema

b. More Problematic symptoms: throat constriction, local- ized edema, wheezing, tachycardia

c. Anaphylaxis: most life-threatening reaction

Chapter 7

I.        Benign: No potential to kill host

II.       Malignant Growth: Can kill host if untreated, invasive/matastasizing nature, grows rapidly

III.      Metastasis: Process by which cancer cells escape their tissue of origin and initiate new colonies of cancer in distant sites

IV.      Effects of Cancer on the Body

a.  Cachexia: Overall weight loss and generalized weakness

i.  Loss of appetitie, increased metabolic rate, nausea/vomiting

b.  Warning signs: Change in bowel/bladder habits, a sore that does not heal, unusual bleeding or discharge, thickening or lump in breast or else- where, indigestion or difficulty swallowing, obvious change in wart or mole, nagging cough or hoarseness

i.  Warning signs in children: continued unexplained weight loss, headaches with vommiting in the morning, increased swelling/per- sistant pain in bones/joints, lump or mass in abdomen, neck or elsewhere, development of whitish appearance in pupil, recurrent fevers not caused by infection, excessive bleeding or bruising, no- ticeable paleness or prolonged tiredness

Module 3

Chapter 51

I.        Contractile Soft Tissue Injuries

a.  Compartment Syndrome: Complication of soft tissue injury, results from swelling of injured tissue within a restrictive fascia

i.  Symptoms: Pain, pallor, parethesia, pulselessness, paralysis

II.       Bone Injuries and Infections

a.  Healing process of bone fracture

b.  Complications of bone fracture: Delayed healing, delayed union, malu- nion, nonunion, compartment syndrome, osteonecrosis, osteomyelitis, neurovascular injury may also occur, deep vein thrombosis,

III.      Metabolic Bone Diseases

a.  Osteoporosis: Most common metabolic disease; occurs when bone re- sorption is greater than bone formation

i.  Pathogenesis

Chapter 52

I.        Local Disorders of Joint Function

a.  Osteoarthritis: Local degenerative joint disorder associated with aging and wear and tear from repetitive stress.

i.  Characterized By: loss of articular cartilage, cartilage calcifies, wear of underlying bone, formation of bone spurs, noninflammatory, weight-bearing joints are often affected

ii. Treatments: *AIMED AT IMPROVING FUNCTION*

1. Physical therapy, reducing pain (acetaminophen/NSAIDS/in- jections of corticosteroids, viscosupplementation, weight re- duction, assistive devices, supportive shoes, total knee or hip surgery.

II.       Acute Gouty Arthritis: Disturbance of uric acid metabolism leads to deposi- tion or uric acid crystals in jointsl risk increases w/ age

b.  *Characterized by hyper uricemia and urate crystal induced arthritis

Chapter 53

I.        Allergic Skin Responses

a.  Contact Dermatitis: cutaneous reaction to topical irritation or allergy; usu- ally results from chemicals or plants

Module 4

Chapter 36

I.        Alterations in the Integrity of the Gastrointestinal Tract Wall

a.  Peptic Ulcer Disease: Disorder of the upper GI tract caused by action of acid and pepsin

i.  Etiology: NSAIDS, stress, smoking, genetics, H. Pylori

1. Gastric: Caused by breakdown of protective mucous layer that normally prevents diffusion of acids into gastric epithelia because of chronic inflammation. (Asprin, NSAIDS, alcohol,& bile acids)

2. Duodenal: Inappropriate excess secretion of acid, increased basal activity of vagus nerve.

ii. Pathogenesis: epithelial cells of the stomach and duodenum se- crete mucus in response to irritation of the epithelial lining and as a result of cholunergic stimulation

II.       Inflammatory Bowel Disease

a.  Ulcerative Colitis: Inflammatory disease of the mucosa of the rectum and colon.

i.  Clinical Manifestations: Bloody and/or chronic diarrhea, passage of mucus, fecal urgency and lower abdominal pain.

b.  Crohn’s Disease: Inflammation of the GI tract that extends through all the layers of the intestinal wall.

i.  Clinical Manifestations: Intermittent bouts of fever, diarrhea, if bloody, not as severe as crohn’s disease. Constant LRQ pain, may have RLQ mass, tenderness.

III.      Enterocolitis

a.  Antibiotic-Associated Colitis (Pseudomembranous Colitis): Acute ind- lammation and necrosis of large intestine. Caused by Clostridium difficile (Exposure to antibiotics) *Medicated by bacterial toxins

i.  Clinical Manifestations: Diarrhea (often bloody), abdominal pain, fever, leukocytosis, sepsis, colonic perforation(rare)

Chapter 27

I.        Infection

a.  Risk factors for UTI’s: female anatomy, sexual activity, menopause, cer- atin types of birth control, Urinary tract abnormalities, blockages in the uri- nary tract, suppressed immune system, catheter use, recent urinary pro- cedure

b.  Acute Pyelonephritis: Infection of renal pelvis/parenchyma usually from ascending UTI

i.  Clinical Manifestations: CVA tenderness, accompanied by fever, chills, N/V, anorexia, which increased fever-induced dehydration

II.       Glomerular Disorders (Glomerulopathies)

a.  Postinfectious acute glomerulonephritis: Immune response to variety of potential triggers. Inflammation results in degradation of the basement membrane.

b.  Clinical Manifestations: Proteinuria, oliguria, azotemia, edema & hyper- tention

c.  Treatment: Supportive measures (dietary & fluid), management of sys- temic and renal hypertension

Chapter 28

I.        Acute Kidney Injury

a.  Prerenal: Due to conditions that diminish perfusion of the kidney

i.  Characterized by: low GFR, oliguria, high urine specific gravity, and osmalality

ii. *can lead to acute tubular necrosis

b.  Intrarenal: due to primary dysfunction of the nephrons and the kidney it- self

c.  Postrenal: caused by obstruction within the urinary collecting system dis- tal to the kidney; elevated pressure in Bowman capsule; impedes glomerular filtration

II.       Chronic Kidney Disease:

III.      Pathophysiology:Outcome of progressive and irrevocable loss of functional nephrons

a.  Complications of CKD: Hypertension & Cardiovascular disease, Uremic syndroma, metabolic acidosis, electrolyte imbalances, bone & mineral dis- orders, malnutrition, anrmia, pain, depression

Chapter 29

I.        Incontinence: Any involuntary Urine loss, never normal, not a part of aging.

a.  Stress Urinary Incontinence (SUI): Occurs when urine is involuntarily lost with increases in intraabdominal pressure

i.  Causes: Weakening of pelvic muscles or intrinsic urethral sphincter deficiency; obesity, childbirth-related trauma, pelvic surgery, dia- betes, degenerative neurologic diseases that impair nerves that in- nervate the bladder

b.  Urgency Urinary Incontinence (UUI): Involuntary sudden leakage of urine alone with or immediately following the sensation of a need to uri- nate (urgency)

Module 5

Chapter 31

i.  Causes: Overactive detrusor muscle, may be idiopathic, bladder in- fection, radiation therapy, tumors or stones, or CNS damage

I.        Male Genital and Reproductive Disorders a.  Acquired Disorders

i.  Priapism: Painful, persistent erection because of engorgement with blood

ii. Phimosis: Uncircumcised foreskin cannot be retracted over the glans of the penis

iii.Paraphimosis: Foreskin that has been retracted over the glans up onto the shaft of the penis cannot be replaced in its normal position

iv. Peyronie’s: Formation of palpable, fibrous plaque on the surface of the corpora cavernose, causing curvature of the penis with painful, incomplete erections

II.       Disorders of the Prostrate

a.  Benign Prostatic Hyperplasia (BPH): As prostate tissue increased, it compressed urethra and bladder outlet

i.  Clinical Manifestations: urinary retention, obstruction to flow, de- creased stream, hesitancy; difficulty initiating a stream, interruption of the stream, infection caused by retention

Chapter 33

I.        Female Genital and Reproductive Disorders

a.  Alterations in Uterine support and Pelvic support

i.  Cyctocele: Protrusion of a portion of the urinary bladder into a weakened part of the anterior vagina

b.  Menstrual Disorders

i.  Menorrhagia: Increase in amount or duration of bleeding; pro- longed and heavy bleeding

Chapter 34

II.       Gonococcal Infection

a.  Etiology:Inflammation of epithelial tissue by organism Neisseria gonor- rhoeae

b.  Clinical Manifestations: pharync, conjunctivae, & anus inflammation

i.  Women: Usually asymptomatic, purulent vaginal discharge, dy- suria, abnormal vaginal bleeding

ii. Men: Dysuria, urethritis, purulent urethral discharge, redness and swelling at infection site

III.      Human Papilloma Virus Infections

a.  Treatment: Prevention and by treating symptoms. Treatment depends on

stage.

Module 6

Chapter 40

I.        Thyroid Hormone Disorders a.  Hypothyroidism

i.  Pathogenesis:

1. Primary: intrinsic thyroid gland dysfunction

2. Congenital Hypothyroididm typically cause by thyroid dys- genesis (lack of development)

3. Secondary: result of defects in TSH production usually asso- ciated with head/brain conditions

4. Lymphocytic thyroiditis, irradiation of the thyroid glans, surgi- cal removal of thyroid tissue, iodine deficiency (required for T3 & T4 formation)

ii. Clinical Manifestations: Decreased basal metabolic rate, weak- ness, lethargy, cold intolerance, decreased appetite, bradycardia, narrowed pulse pressure, mild/moderate weight gain, elevated serum cholesterol & triglycerides, enlarged thyroid, dry skin, consti- pation, depression, difficulties with concentration/memory, loss of eyebrow, menstrual irregularity

b.  Hyperthyroidism

i.  Clinical Manifestations: Insomnia, restlessness, tremor, irritability, palpations, heat intolerance, diaphoresis, diarrhea, inability to con- centrate, enlarged thyroid gland, Increased basal metabolic weight which leads to weight loss even with increase in appetite and di- etary intale, amenorrhea/scant menses

II.       Parathyroid Hormone Disorders

a.  Hypoparathyroidism

i.  Clinical Manifestations: kidney stones, bone demineralization (os- teoporosis), polyuria & dehydration, anorexia, vomiting, constipa- tion, bradycardia, heart block, cardiac arrest, decrease in neuro- muscular excitability.

III.      Antidiuretic Hormone

Chapter 41

I.        Diabetes Mellitus a.  Type I Diabetes

i.  Pathogenesis: caused by destruction of beta cells of the pancreas

ii. Clinical Manifestations: hyperglycemia, polyuria, polydipsia, polyphagia

b.  Type II Diabetes

i.  Pathogenesis: Insulin resistance and beta cell dysfunction lead to a relative lack of insulin

ii. Clinical Manifestations: Acute hyperglycemia, dawn phenome- non, pulyuria, polydipsia, polyphagia, nausea, fatigue, blurred vi- sion

II.       Clinical Manifestations and Complications a.  Vascular complications

i.  Macrovascular: damage to large blood vessels; leads to cardio- vascular disease, peripheral vascular disease, and stroke

ii. Microvascular: retinopathy and nephropathy from abnormal thick- ening of the basement membrane in capillaries; may lead to blind- ness and renal failure

III.      What is a Hemoglobin AIC?

Evaluated the average amount of glucose in the blood over the last 2-3 months by measuring the percentage of glycared hemoglobin in the blood

Module 7

1.  Manifestations of Brain Injury

a.  Level of Consciousness: State of alertness and attentiveness to one’s enviornment and situation

a.  Change in level of conciousness is most sensitive indicatior of al- tered brain function

b.  Glasgow Coma Scale: Standardized tool for assessing LOC in acutely brain-injured persons

a.  Mild( greater than 12), Moderate (9 to 12), severe (less than 8)

c.  Decorticate Posturing

d.  Decerebrate Posturing

2.  Cerebrovascular disease and Stroke

a.  Ischemic Stroke: results from sudden occulusion of cerebreal artery sec- ondary to thrombus formation or embolu

i.  TIA’s: Symptoms typically last only minutes, but they may last as long as 24 hours. Important warning signs of thrombotic disease and carry significant risk for subsequent stroke

b.  Hemorrhagic Stroke: Hemorrhage within the brain parenchyma, common in basal ganglia or thalamus

c.  Stroke Sequela

i.  Motor and sensory deficits: initially motor deficite occur as flac- cidity or paralysis; recovery of motor function occurs wth onset of spasticity

ii. Language deficits: Aphasia occurs with brain damage to dominant cerebreal hemisphere and can involve all language modalities

iii.Cognitive deficits: language impairments, impaired spatial rela- tionship skills and short-term memory and poor judgement, concen- tration, memory and reasoning may be inpaired.

3.  Cerebral Aneurysm: Lesion of an artery that results in dilation and ballooning of a segment of the vessel

4.  Central Nervous System Infections

a.  Meningitis: Bacteria usually reach the CNS via the bloodstream or exten- sion from cranial structures like sinuses or ears

a.  Streptococcus pneumoniae

b.  Bacteria invade leptomeninges; accumulation of inflammatory exu- date can result in obstructive hydrocephalus

b.  Encephalitis: Inflammation of the brain commonly caused by West Nile virus, western equine encephalitis and herpes

5.  Brain and Cerebellar Disorders

a.  Seizure disorder (Epilepsy): transient neurologic event of paroxysmal abnormal or excessive cortical electrical discharges

b.  Dementia: Syndrome associated with many pathologies; characterized by progressive deterioration and coninuing decline of memory and other cog- nitive changes

c.  Parkinson disease: difficulty initiating and controlling movements, results in akinesia, tremor, and rigidity

6.  Spinal cord and peripheral nerve disorders

a.  Multiple sclerosis: Chronic demyelinating disease of the CNS that pri- marily affects young adults

b.  Spinal cord injury: Usually traumatic, cord may be compressed, tran- sected, or contused. Secondary injury may result from hemorrhage, swelling, ischemia, inflammation

c.  Guillian-Barre syndrome: Inflammatory demyelinating disease of the pe- ripheral nervous system or a lower motor neuron disorder

Module 8

1.  Alterations in Pulmonary Function

a.  Hypoxemia: deficient blood oxygen as measured by low artetial O2 and

Low hemoglobin saturation

b.  Hypoxia: decrease in tissue oxygenation

2.  Diagnostic tests

a.  Pulmonary function testing

3.  Alterations in Pulmonary Vasculature

a.  Pulmonary venous thromboembolism: An undissolved, detaches material (blood clot, fat embolu, amniotic fluid, air, tumor, foreign bodies, septic, parasites) that occludes blood vessels

a.  90% in deep veins of lower extremeties

4.  Obstructive Pulmonary Disorders

a.  Obstruction From Conditions in the Wall of the Lumen

i.  Asthma: Airway obstruction/ inflammation that is reversible

i.  Intrinsic: Non-allergic, Adult onset

ii. Extrinsic: Allergic, Pediatric onset

ii. Chronic Bronchitis: Acute inflammation of the trachea and bronchi with chronic or recurrent productive cough

b.  Obstruction Related to Loss of Lung Parenchyma i.  Emphysema:

ii. Clinical Manifestations: Progressive, exertional dyspnea, thin, use of accessory muscles, pursed-lip breathing, cough (minimal or absent), digital clubbing, barrel chest

5.  Restrictive Pulmonary Disorders a.  Atelectatic Disorders

i.  Infant Respiratory Distress Syndrome:

b.  Pleural Space Disorders

i.  Pneumothorax: Air enters during inspuration but cannot escape during expiration leafs to shift of mediastinum

i.  Results from buildup of air under pressure in pleural space

c.  Infection or Inflammation of the Lung

i.  Pneumonia: Inflammatory reaction in the alveoli and intersitium caused by an infectious agent

1.  Viral: Upper Respiratory Prodrome

1.  Dever, nonproductive cough, hoarseness, coryza ac- companied by wheezing/rales

2.  Bacterial:

ii. Pulmonary Tuberculosis:

i.  Clinical Manifestations: History of contact w/ infected per- son, low-grade fever, chronic cough, night sweats, fatigue, weight loss, malaise, anorexia, apical crackles (rales), bronchial breath sounds over region of consolidation, mal- nourished

ii. Etiology: Inhalation of small droplets containing bacteria, droplets expelles with cough, sneeze or talking

Module 9

Chapter 13

I.        What is erythropoietin?

a.  Hormone Produced by the kidney

b.  Promotes the formation of red blood cells by bone marrow

c.  Can be synthesized and used as a treatment of some forms of anemia

II.       Anemia: Deficit of red blood cells

a.  General Effects of Anemia: Reductions in oxygen-carrying capacity (Tis- sue Hypoxia)

i.  Mild Anemia: usually no clinical symptoms, Elderly with cardiovas- cular, pulmonary disease ,ay have symtoms

ii. Mild to Moderate Anemia: Fatigue, Generalized Weakness, Loss of stamina, followed by tachycardia and xertional dyspnea.

iii. Moderate to Severe Anemia: Orthostatic and generalized hy- potension, vasoconstriction, pallor, tachypnea, dyspnea, tachycar- dia, transient murmurs, angina pectoris, heart failure, intermittent claudication, night cramps in muscles, headache, lightheadedness, faintness, tinnitus, roaring in the ears

b.  Aplastic Anemia

i.  Etiology: Caused by toxic, radiant, or immunologic injury to red blood cells (Immune systems attacking stem cells in blood marrow)

ii. Pathogenesis:

1. Late Symptoms: weakness, fatigue, lethargy, pallor, dysp- nea, palpitations, transient murmurs, and tachycardia related to low RBC’s

c.  Iron Deficiency Anemia

i.  Clinical Manifestations: Pica, Blue Sclerae, Koilonychias (spoon- shaped nails)

d.  Sickle Cell Anemia

i.  Pathogenesis: caused by mutation in the beta-globin chain of the hemoglobin molecule

e.  Acute Blood Loss

i.  Clinical Manifestations:

1. 10%: rarely causes signs, other thn vasovagal syncope

2. 20%: no clinical symptoms at rest, tachycardia is seen with exercise

3. 30%: flat neck veins when supine, postural hypotension, exercise tachycardia

4. 40%: central venous pressure, cardiac output, & arterial blood pressure to fall below normal while patient is supine and at rest; with associated hunger, tachycardia, and cold, clammy skin

5. 50%: causes shock and often death

ii. Treatment: blood replacement therapy, w/ crystaloid solutions colloid solutions (Plasma protein, albumin, or dextran)

f.   Polycythemia Vera

i.  Pathogenesis

ii. Clinical Manifestations g.  Secondary Polycythemia

i.  Etiology: Caused ny chronic hypoxemia with resultant increase in erythropoietin production

Chapter 14

II.       Vascular and Platelet Disorders a.  Thrombocytopenia

i.  Etiology: Bone marrow supression from chemotherapy, recent im- munizations, alcohol ingestion

ii. Clinical Manifestations: Low platelet count (below 20,000 cells/uL, prolonged bleeding time, easy bruising, bleeding gums, occult hematuria, retinal hemmorrhages, petechiae (purple, red, brown spots on skin), purpura(blood spots or skin hemmorrhages)

b.  Disseminated Intravascular Coagulation (DIC): Acquired hemmorhagic syndrome in which clotting and bleeding occur sumultaneously

i.  Etiology: Trauma, malignancy, burns, shock, abruptio placentae

ii. Clinical Manifestations: Widespread clot formation in small ves- sels; clotting factors and platelets consumed can result in bleeding

c.  Hepatic Disease

i.  Pathogenesis

Chapter 11

I.        Chronic Myeloid Leukemia a.  Pathogenesis

b.   Clinical manifestations

II.       Leukemia

a.  Prevention and Management of Complications

III.      Bone Marrow Transplants

Module 10

Chapter 18

a.  Risk Factors of Coronary Atherosclerosis

III.      Clinical Features and Management of Coronary Syndromes a.  Angina Pectoris

i.  Clinical Features:

ii. Management:

IV.      Acute Coronary Syndrome a.  Clinical Features:

b.  Management

c.  Serum biomarkers

V.       Endocardial and Valvular Diseases

a.  Valve stenosis vs. regurgitation: stenosis, the valve narrows, restrict- ing blood flow from the heart. In aortic regurgitation, the valve open- ing does not close completely, causing blood to leak backward into the heart.

b.  Rheumatic Heart Disease

Chapter 15

I.        Arteriosclerosis/Atherosclerosis: “Hardening of the arteries”

a.  Risk Factors

i.  Modifiable: Smoking, elevated blood pressure, glucose intoler- ance, elevated cholesterol & low-density lipoproteins, decreased physical activity, obesity, weight fluctuations, ineffective stress man- agement

ii. Non-modifiable: Age, gender, ethnicity, heredity

b.  Peripheral Artery Disease

i.  Clinical Manifestations

II.       Alterations in venous flow

a.  Chronic Venous Insufficiency

i.  Clinical Manifestations and Treatment

Chapter 16

II.       What is Mean Arterial Pressure? III.      Primary Hypertension

a.  Atherosclerosis

i.  Outcomes-End-organ damage ii. Treatment Interventions

IV.      Low Blood Pressure

a.  Orthostatic hypotension