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Pathophysiology Final Exam Study Guide Modules 1-10 Correctly Verified, Study Guides, Projects, Research of Nursing

Pathophysiology Final Exam Study Guide Modules 1-10 Correctly VerifiedPathophysiology Final Exam Study Guide Modules 1-10 Correctly VerifiedPathophysiology Final Exam Study Guide Modules 1-10 Correctly VerifiedPathophysiology Final Exam Study Guide Modules 1-10 Correctly VerifiedPathophysiology Final Exam Study Guide Modules 1-10 Correctly VerifiedPathophysiology Final Exam Study Guide Modules 1-10 Correctly Verified

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Pathophysiology Final Exam Study Guide
Modules 1-10 Correctly Verified
odule 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
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
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Download Pathophysiology Final Exam Study Guide Modules 1-10 Correctly Verified and more Study Guides, Projects, Research Nursing in PDF only on Docsity!

Modules 1-10 Correctly Verified

odule 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

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

Modules 1-10 Correctly Verified

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-

Modules 1-10 Correctly Verified

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

Modules 1-10 Correctly Verified

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

Modules 1-10 Correctly Verified

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)

Modules 1-10 Correctly Verified

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

Modules 1-10 Correctly Verified

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

Modules 1-10 Correctly Verified

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

Modules 1-10 Correctly Verified

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

Modules 1-10 Correctly Verified

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

Modules 1-10 Correctly Verified

ii. Pathogenesis:

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,

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

Modules 1-10 Correctly Verified

II. Coronary Heart Disease

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

Modules 1-10 Correctly Verified