Nursing 225 - Patho (Exam 1)

Etiology

what causes the disease (risk factors, genetics, environment)

Pathogenesis

How does it evolve

Clinical

What someone looks like when they have symptoms

Diagnosis

labs, tests, findings

Treatment

medications, surgery, nursing care

Nursing

What we need to watch for (what affects us as nurses)

Homeostasis

Mechanisms to maintain internal body parameters in balance and stable

Homeostasis examples:

pH -

Blood glucose -

Serum electrolytes -

Core temperature -

Serum osmolarity -

pH - acid/base balance - controls cell function

Blood glucose - brain needs constant supply

Serum electrolytes - dissolve into ions; body needs for systems - cardiovascular and neuro

Core temperature - keep body in optimal temp

Serum osmolatiry - amount of solute in plasma - concentrated or diluted

Control of Blood Glucose levels

Blood glucose concentration rises: pancreas secretes more insulin and less glucagon; cells remove glucose from blood and convert to glycogen; blood glucose falls

Blood glucose concentration falls: (hypoglycemia) pancreas secretes less insulin and more glucagon; cells convert glycogen to glucose and release it into the blood; blood glucose rises

Stress

State manifested by a specific syndrome of the body developed in response to any stimuli that made an intense systematic demand on it

*anything that is perceived as challenging or threatening

*if too much can become a disease to the body

General Adaptation Syndrome (3 stages)

Alarm

Resistance

Exhaustion

Alarm stage

*Body systems activated in response to threat

*Activation of sympathetic Nervous System (SNS) - fight or flight

What happens when the SNS is activated

Release of catecholamines - from adrenal glands to blood stream

What are two catecholamines related to the SNS

Epinephrine and Norepinephrine

What does Epinephrine effect

A1 - vascular smooth muscles and blood vessels --> constrict (increase BP and divert blood flow to the core of body)

B1 (1 heart) - increase heart rate and increase force of contractions

B2 (2 lungs) - bronchodilates (relaxes muscles in the bronchi)

What does Norepinephrine effect

Primarily acts on A1 - vascular smooth muscles and blood vessels - constriction --> increases BP and diverts blood flow to core of the body

True or False

Activation of Hypothalamic-Pituitary Adrenal (HPA) axis occurs in the Alarm Stage

True

*senses stress and releases cortisol to withstand the stress placed on the body

*release of cortisol - want more glucose available for energy

Cortisol

*Inhibit tissue (protein) building

*encourage fluid retention

*inhibit CRH and other when enough cortisol

Activation of Renin-Angiotensin-Aldosterone System (RAAS)

*Part of the Alarm stage

*Helps to increase BV and increase vasoconstriction

Parasympathetic (break)

*rest and digest

*decrease in heart rate

*bronchoconstriction

SLUDD

*with Parasympathetic

*S - salivation

*L - Lacrimation

*U - Urination

*D - Digestion

*D - Defecation

Sympathetic

*fight or flight

*dilates pupil

*increase heart rate

*bronchodilation

*secretions/peristalsis inhibited

*glycogen to glucose

*inhibition of bladder contraction

Effects of catecholamines

*decreased insulin secretion - want more glucose

*increased glucagon release

*increased heart rate and myocardial contractility - more cardiac output --> increase blood flow

*increased vascular smooth muscle tone - constrict blood vessels

*bronchial smooth muscle relaxation - dilation of bronchials

*chronically elevated levels of NE results in increased production of inflammatory leukocytes which adhere to vessel walls and promote antherosclerotic plaque formation - leukocytes (WBCs)

Effects of Cortisol

*makes epinephrine more stimulating to heart, vessels and bronchials - potentiates effects of epinephrine and glucagon

*enables more energy to be available to cells --> excess amounts affect wound healing, muscle wasting and falling apart of skin

More Effects of Cortisol

*Suppress release of inflammatory cytokines and immune system

*suppresses protein and collagen synthesis

*gluconeogenesis from proteins and fats - convert protein and fat to glucose (can't store energy and build tissue)

*if chronically elevated contributes to insulin resistance, obesity and CV disease

*make more insulin and bring back into range

RAAS

*Renin-Angiotensin-Aldosterone-System

*Kidney (releases renin because not enough blood flow) --> angiotensinogen (liver) --> angiotensin I (lungs) --> angiotensin II

Angiotensin II has 2 effects

*vasocontricts - Increases blood volume and BP

*Aldosterone - hold onto sodium and water

End result of RAAS Activation

*Vasoconstriction

*Sodium and Fluid Retention

*potassium excretion

*increased BP

Individual Variations in Stress Response

*age - young vs old

*genetics - predisposed

*physiological reserve - how much extra do organs have to handle (baseline status of organ function)

*prior life experiences

*coping strategies - stress and how do you process

*social support

*diet

Coping with Stress

*Adaptive and Maladaptive coping strategies

Adaptive Coping with Stress (friends and families)

*social support

*exercise

*meditation

Maladaptive Coping with Stress

*drinking

*smoking

*binge eating

*poor sleeping

Impact of chronic stress response

Allostatic Overload

Allostatic overload

Stress experiencing leads to body dysfunction

*immune system effects

*hypertension

*cardiac remodeling

*increased risk of Cardiovascular disease

*diabetes

*mental health issues

*substance abuse

Immune system effects (of allostatic overload)

*Decreased innate immunity - body can't destroy pathogens easily (gets colds easily)

*Upregulated adaptive immunity - reliant on antigen-antibody reaction - cause autoimmune disease

*increase inflammation

Post-Traumatic Stress Disorder (PTSD)

Severe stress response to experiencing a traumatic event

*war

*natural disaster

*rape

*trauma

Pathophysiology for PTSD

Exaggerated chronic stress response with elevated neuroendocrine response

Clinical Manifestations of PTSD

*Intrusion - can't get away from thoughts of traumatic events (flashbacks and nightmares)

*Avoidance - socially disconnected (numbing of emotions, guilt and depression)

*Hyperarousal -feeling on edge/look for threats (difficulty concentrating, hypervigilance, exaggerated startle)

PTSD Diagnosis

Clincial - experience of traumatic even

*presence of intrusion, avoidance and hyperarousal for at least one month

*clinically significant distress

PTSD prevention and Treatment

Prevention - cope immediately and debriefing traumatic events

Treatment - recognition (depression, anxiety, substance abuse may indicate PTSD), cognitive therapy (talk therapy), antidepressants, developing healthy coping strategies

Which of the following is not a physiological response to stress?

A. an increase in cortisol levels

B. An increase in catecholamines

C. an increase in blood pressure

D. a decrease in inflammatory response

D. a decrease in inflammatory response

In which stage of the General Adaptation Syndrome is the sympathetic nervous system response initiated?

A. Alarm

B. Resistance

C. Exhaustion

D. All of the above

A. Alarm

Which of the following physiological responses are evident in the stress response (select all that apply)

A. Secretion of Norepinephrine

B. An increased level of ACTH

C. Increased release of insulin

D. Vasodilation

E. Increased Cardiac Output

A. Secretion of Norepinephrine

B. An increased level of ACTH

E. Increased Cardiac Output

Stimulation of the parasympathetic nervous system would have which of the following effects?

A. Decreased salivation

B. Increased intestinal motility

C. Increased heart rate

D. Bronchodilation

B. Increased intestinal motility

Stimulation of the renin-angiotensin aldosterone system has which of the following physiological effects?

A. Vasodilation

B. Decreased serum potassium

C. Decreased BP

D. Fluid excretion

B. Decreased serum potassium

When cortisol levels increase what is the effect on the hypothalamus and pituitary?

A. Increased secretion of CRH and ACTH

B. Decreased secretion of CRH and ACTH

C. Increased secretion of CRH and decreased secretion of ACTH

D. Decreased secretion of CRH and increased secretion of ACTH

B. Decreased secretion of CRH and ACTH

The nurse is taking a history on a combat veteran. All of the following client statements would support a diagnosis of PTSD EXCEPT:

A. "I have been anxious for the past two weeks"

B. "I feel disconnected from my wife"

C. "I have recurrent nightmares about being shot at"

D. "I can't finish reading a book chapter without getting distracted"

A. "I have been anxious for the past two weeks"

Inflammation

Physiological response to tissue injury, infection, or the presence of a foreign body

*mediated by inflammatory chemicals

Cytokines

Inflammatory chemicals - released and regulated by White Blood Cells

Purpose of Inflammation

Remove microorganisms, necrotic tissue, and initiate tissue repair

Cardinal signs of inflammation

*Redness

*Swelling

*Heat

*Pain

*Loss of Function

Acute Inflammation - Vascular Phase

Vasodilation at site of injury (chemicals and cells to area - more blood flow)

*increase blood flow to area and produces heat and redness

Increased capillary permeability - open up and allow cells needed for tissue repair to get to area

*outflow of protein rich fluid into interstitial spaces

*protein in exudate pulls in additional fluid by osmosis

*produces swelling, pain, loss of function

*White Blood Cells to enter area

Acute Inflammation - Cellular Phase

*activated platelets release inflammatory mediators

*Neutrophils migrate to area of injury -- elevate with long term injury

Neutrophils

*White Blood Cells 1st responders

*Typically within 6-12 hours

*Phagocytosis - digest debris and bacteria

*Lifespan of 10 hours

Monocytes

*secrete additional inflammatory mediators (chemicals)

*macrophages can engage in phagocytosis for several days - when enter interstitial area --> mature

Mast Cells

degranulates and release chemical histamine

Chemical Mediators Involved in Inflammation - Arachidonic Acid Metabolites

Prostaglandins -- acute soft tissue injury

*induces vasodilation (redness and swelling) and bronchoconstriction

Leukotrienes - asthma, bronchospasm in lung

*induces bronchoconstriction and microvascular permeability (swelling/edema)

*synthesized from Leukocytes - White Blood Cells especially macrophages

Chemical Mediators Involved in Inflammation - Bradykinin

Activated from Plasma Proteins

*increases vascular permeability

*induces smooth muscle contraction - mostly bronchial constriction

*dilates blood vessels

*increases pain sensitivity

Chemical Mediators Involved in Inflammation - Histamine

Released by Mast Cells

Results in transient vasodilation in acute phase of inflammatory reactions

Binds to H-1 receptors - triggers response in body to histamine

Chemical Mediators Involved in Inflammation - Complement System

*helps antibodies to get rid of pathogens with inflammation

*Plasma proteins

*Functions

**Opsonization - immune system identify cell as foreign; marked for destruction by opsonization

**stimulation of mast cell degranulation

**Leukocyte chemotaxis - draw WBC to injury to infection

**Cell lysis

Chemical Mediators Involved in Inflammation - IL-1 and TNF-alpha

*interleukin 1 and tumor necrosing factor

*released from activated macrophages

*effect endothelial cells to express adhesion molecules and release additional cytokines and chemokines

*initiates acute phase response - fever, release of more neutrophils, hpotension, tachycardia, anorexia, malaise, release of cortisol; increased synthesis of inflammatory protein in liver

*systemic reaction to infection - affect vascular system and HR decreases

Chronic Inflammation

*results from unresolved injury, infection or foreign body

*macrophages (predominant cell), lymphocytes and fibroblasts predominate instead of neutrophils

*presence of fibroblasts (drawn to area) increases the risk of scarring and deformity

Granuloma

Macrophages surrounded by lymphocytes "wall off" the foreign protein (latent tuberculosis)

*scar tissue to wall off infection

Abscess

*Fibroblasts (form tissue) wall off area to infection

*antibiotics will not penetrate

*requires incision and drainage (I&D)

*once forms has to be drained or won't be resolved

Inflammation and Disease

Uncontrolled or inappropriate inflammation can cause tissue damage

*Rheumatoid Arthritis - autoimmune disease (destroys joint structures)

*Sepsis - inflammation impairs ability to perfuse

*Inflammatory Bowel Disease - against colon - tissue damage

White Blood Cell Count Differential

Breaks down each type of cell - high to low

Neutrophils

*40-70% of WBCs under normal condition

*primary initial phagocytosis in acute injury or infection

*short life span

Eosinophils

*1-6% of total WBC count

*Associated with an increase in number during allergic reaction and infection by intestinal parasites

*Release inflammatory chemicals in areas of inflammation

*Primary function is to kill parasitic helminths (worms)

Basophils

*0-2% of total WBC count

*Release vasoactive substances (heparin, histamine) during inflammation

Monocytes

*Immature macrophages

*5% of total WBC count

*Circulate in the blood stream for about 3 days prior to entering tissue and becoming macrophage

Macrophages

*Remain in tissue for long time

*called different cells in different tissues

*lifespan from months to years

Functions of Macrophages

Phagocytosis

Repair of injured tissue - fibroblasts

Antigen processing - CD4+

Secretion of cytokines to help control the immune system

Secrete growth factors to stimulate angiogenesis and fibroblasts - development of new capillaries/blood vessels

*to bring in fibroblasts

Lymphocytes - NK cells

*innate immune cells

*can kill tumor cells and virally infected cells without previous exposure

*don't need to be exposed to be killed

Lymphocytes - T cells

*Major cells of cell-mediated immunity

*T-helper cells (CD4+)

*Interact with antigens

*Secrete cytokines that stimulate B-cell proliferation and antibody production

*exposed to have body respond

Lymphocytes - B cells

B cells

*major cells of antibody-mediated immunity

*able to produce antibodies

*require help from T helper cells to respond

*need to be initiated by T cell

Differential White Blood Cell Response to Infection - Bacterial Infection

*acute injury

*increase in neutrophils or the measure of immature neutrophils

*if severe may include immature neutrophils "bands" - bone marrow working over time to create more neutrophils (severe infection)

*"LEFT SHIFT"

Differential White Blood Cell Response to Infection - Viral Infection

*decrease in neutrophils

*increase in lymphocytes

Tissue Regeneration

Tissue varies in ability to replace itself with functional cells

*Labile cells - can be replace easily -- continuously divide and can be replaced (mucosal linings, bone marrow, oral cavity)

*Stable cells - maintain steady state unless trauma, if trauma they can regenerate -- stop dividing when growth ceases but can regenerate when needed (parenchymal cells of liver and kidney, vascular endothelium)

*Permanent cells - can't regenerate (nerve cells, myocardial cells - stroke and heart attack)

Wound Healing Process - Inflammatory Phase

*Initial Process

*localized inflammation

*neutrophils arrive - begin phagocytosis of bacteria and debris

*Macrophages - arrive after 24 hours; continue phagocytosis; release growth factors that stimulate epitheliazation (regeneration of skin), angiogenesis (blood vessels) and attract fibroblasts (collagen)

Wound Healing Process - Proliferate Phase

Granulation - sign wound healing and producing healthy tissue

*Fibroblasts synthesize collagen and growth factors which induce angiogenesis

*for granulation to occur necrotic tissue must be removed

Hypergranulation

Excessive granulation tissue that extends above the wound edges and prevents healing

Epitheliazation

Skin grow, come together and close

*migration of epithelial cells to close surface of wound

Wound Healing Process - Remodeling Phase

*happens underneath the surface

*collagen scar reorganizes and strengthening

*continues for up to 2 years

*scars never regain full tensile strength as old tissue

Keloid

abnormal scar tissue formation - excessive formation of scar tissue

*more common in African Americans

Primary Intention (Wound Healing)

*Superficial, surgically

*heal better and faster

*edges approximated - created

*surface epitheliazation - heal with skin itself

Secondary Intention (Wound Healing)

*Deeper wounds

*Heels bottom up by granulation

*longer, more complicated, scarring

Things needed for effective wound healing

*removal of necrotic (infected) tissue

*control of infection

*moist wound bed - capillaries generated better and better granulation

*adequate nutrition - protein, vitamins and calorie intake will help with tissue repair

*Adequate oxygen delivery - oxygenation, perfusion (poor blood flow to wound), hemoglobin

Causes of impaired wound healing

Malnutrition - protein (wound healing/tissue building), carbohydrate (energy), Vitamin A, C, and Zinc

Vascular Disease - arterial disease -- poorly perfused; difficult to get nutrients and oxygen to tissue and wound

Diabetes - decreased Oxygen (b/c of glucose levels), Microvascular Disease (poor capillary perfusion), impaired Leukocyte function (wounds infected)

Hypoxia - low levels of oxygen

Smoking - decreased oxygenation and hypercoagulability (blood more sluggy; poor perfusion)

medications - steroids (pharmacologic cortisol) and chemo (attacks cell division)

Why would corticosteroids impair wound healing?

Cortisol helps to increase glucose - which in turn inhibits protein synthesis used to help wound healing

Types of Wounds

*Surgical

*Traumatic

*Pressure Ulcers

*Burns

*Arterial Ulcers

*Venous Stasis Ulcer

Surgical Wounds

Complication - infection

*redness, drainage (perulent - pussy)

Wound Dehiscence

Wound separates (pops open)

*sensation of "giving away"

*risk factors - obesity (hard to get good closure), diabetes, malnutrition

*Precipitating factors - sudden straining - pressure of action; splint incision (hold something against wound for less stress

*Management - cover wound, notify surgeon

Evisceration

Wound dehiscence that organs come through wound

*surgical emergency

*cover with sterile saline towels or dressings

*keep NPO - Nothing by Mouth

*prep for surgery

Traumatic Wounds

Laceration - tearing of tissue; may require suturing (depending on depth)

Abrasion - scraping of superficial layer

Contusion - blunt trauma (may not break skin but tissue damage underneath); bruising/hematoma

Puncture - deep cavity created (deep tunnel created)

Traumatic Wound Management

*Control Bleeding - hold pressure w/ gauze (elevated above heart level)

*Cleanse wound of foreign material - sterile saline

*Assess wound - size and dimension, need for closure

*Update tetanus vaccine - w/ booster - especially for puncture wounds

*Educate patient - wound care, signs and symptoms of infection - purulent drainage, redness, swelling, fever

Pressure Ulcers

Skin breakdown caused by unrelieved pressure against body (skin against bone - cut off circulation and decrease blood flow to area)

*also called Decubitus Ulcer/Bed sore

*Pressure, usually over bony prominences, cuts off circulation to skin and underlying tissue resulting in ischemia (inadequate blood flow to area), necrosis and breakdown

*capillary pressure is 25-35 mm Hg anymore and capillary cuts off

Causative Factors

*Decrease ability to withstand pressure

*interplay between compressive pressure and tissue resilience - history of patients tissue and skin

*friction

*shear - layers of tissue separate in opposite directions

*duration of pressure

*decreased tissue tolerance - underlying history of tissue

Areas of greatest risk

Heels

Sacrum

Coccyx

Trochanters - hips

Ischium - Butt

Factors which reduce tissue resistance to pressure

*Aging - older tissue

*Diabetes - impairs tissue building and wound healing

*Moisture/Incontinence - breaks down skin (feces and urine)

*vascular disease

*malnutrition - albumin levels -- plasma protein (low indicates poor nutrition and protein deficit)

*dehydration

Risk Factors

Paralysis/Immobility - can't move on own

Orthopedic Surgery - pain from surgery

Confusion/Sedation

Impaired Sensation - neuropathy can't feel skin breakdown

CHF (heart failure), PVD, COPD, diabetes, malignancy

Elderly