Pathophysiology Exam 1

Buffer Systems

• Mix acids and bases to prevent changes to pH levels

• Trade stronger acids and bases for weaker ones

• Three types are renal, respiratory, and through plasma

Pathogen

• Disease-causing microorganism

• Types: Obligate vs facultative, bacteria, viruses, rickettsiae, mycoplasmas, and chlamydiae, fungi, protozoa, helminths

Factors Affecting Pathogenicity

• Virulence (severity)

• Infectivity (ease of ability of an organism to infect a host)

• Toxigenicity (ability to produce toxins)

• Antigenicity (ability to be recognized by the immune system)

• Coinfection (simultaneous infection with greater than one infection species)

• Superinfection (secondary infection that occurs after an initial infection, usually caused by a different microbial agent. The second infection is often resistant to the treatment used for the first

Multifactorial

Having more than one cause

Idiopathic

Having no known cause

Nosocomial

Caused by an infection received in a healthcare environment

Iatrogenic

Caused inadvertently by medical treatment

Signs

Something you can see

Symptoms

Something that is complained about

Primary prevention

Prevention of a disease occurring

Secondary prevention

Prevention of a disease by screening

Tertiary prevention

Rehabilitation of a patient to prevent complications or progression of disease

Trousseau’s sign

A sign of hypocalcemia. Carpal spasm caused by inflating a blood pressure cuff above the client’s systolic pressure and leaving it in place for 3 minutes.

Chvostek’s sign

Cheek, facial spasm when cheek is tapped associates with hypocalcemia

Cations

Positvely charged ions

Anions

Negatively charged ions

What processes do fluid balance within the body?

Through osmosis, reabsorption, and filtration

Ways to regulate fluid balance in the body?

Thirst, renin angiotensin-aldosterone system (RAAS), antidiuretic hormone (ADH), diuretics

Hydrostatic force

• Water pressure from within the blood vessels, moving from high to low

• Bodily fluid balance force

• At the beginning of the capillary, arterial side, where capillary hydrostatic pressure is highest, hydrostatic force is dominant and pushes fluid out of the blood vasculature and into the interstitial fluid

Osmotic force

• Water pressure that moves against the concentration gradient to hold water on one side

• Bodily fluid balance force

• Driven by plasma proteins and interstitial fluid pressure

• Mainly reabsorption, becomes dominant on venous end and draws fluid back into the capillaries from interstitial space

Fluid regulation

• Thirst

• Renin-angiotensin-aldosterone (RAAS)

• Antidiuretic hormone

• Diuretics

Tonicity

• Isotonic: solution osmolality (conc. levels) are equal on either side of the plasma membrane, so volume remains unchanged on both sides

• Hypotonic: water moves into the cell down its concentration (osmotic) gradient, and the cell swells

• Hypertonic: the osmotic gradient is directed outward causing water to leave the cell and it shrinks

Dehydration

• Alteration in fluid and electrolyte balance, sodium imbalance, negative fluid balance

• Causes can include decreased fluid intake, increased fluid output, fluid shift between compartments (ascites)

• Classification:

  • Hyponatremic

    • sodium concentration (<130mEq/L)

    • frequency of diagnosis (5-10%)

    • type of fluid loss (hypertonic)

    • fluid shifts (none)

  • Isonatremic

    • sodium concentration (130-150mEq/L)

    • frequency of diagnosis (80%)

    • type of fluid loss (isotonic)

    • fluid shifts (none)

  • Hypernatremic

    • sodium concentration (>150mEq/L)

    • frequency of diagnosis (5-10%)

    • type of fluid loss (hypotonic)

    • fluid shifts (extravascular to intravascular)

Dehydration manifestation

• decreased level of consciousness

• prolonged capillary refill time

• dry mucous membranes

• decreased or absent tears

• change in vital signs

• depressed fontanel (sunken areas that allow for compression in baby skull), sunken eye

• decreased or absent urine output

Dehydration diagnostic criteria

- History and physical examination including fluid intake/output, nutrition, and characteristics of urine, stool, emesis, and sweat

- Lab analysis including blood concentrations of electrolytes, bicarbonate, blood urea nitrogen, creatinine, and specific gravity

Dehydration treatments

- Rehydration either orally or through IV

- Correction of electrolyte imbalance

Metabolic alkalosis

- Increased pH caused by plasma excess of HCO3−

- Contributing mechanisms are decreased H+ ions, increased HCO3− ions, and loss of Cl− ions

- Clinical manifestations: Asymptomatic, signs related to hypokalemia

- Lab findings: pH >7.45, HCO3− >31 mEq/L

Appropriate pH Range

- 7.35 to 7.45

Metabolic acidosis

- A base deficit of HCO3−

- Contributing mechanisms include increased production of nonvolatile acids, decreased secretion of acids by kidneys, increased loss of bicarbonate, increase in Cl−

- Clinical manifestations: Anorexia, nausea, vomiting/emesis, weakness, lethargy, confusion, coma, vasodilation, decreased heart rate, and flushed skin

- Lab findings: pH <7.35, HCO3− <24 mEq/L

Acids

substances that donate hydrogen ions

Bases

substances that accept hydrogen ions

Plasma (buffer system)

reacts in seconds to hydrogen ion levels

Respiratory (buffer system)

reacts in minutes to excrete CO2

Renal (buffer system)

reacts in hours to days to produce, absorb, and excrete acids, bases, and ions

Body’s first line of defense

surface and chemical barriers

Body’s second line of defense

waged through an effective inflammatory response

Body’s third line of defense

activated through the immune response

Risk factors for altered immunity

- Diabetes

- High BMI

- Open Skin

- Excessive Age (over 60)

Cells involved in immunity

- T Lymphocytes

- B lymphocytes

- Natural killer cells

T lymphocytes

- Mature in Thymus

- Involved in cell-mediated immunity

- Make cytotoxic, helper, and suppressor T cells

B lymphocytes

- Mature in Bone marrow

- Produce antibodies

- Make memory cells/plasma cells

Immune defense map

- Innate immunity is non-specific

- Adaptive immunity is specific

NLMEB

Pneumonic for WBCs, neutrophils, lymphocytes, monocytes, eosinophils, basophils.

Never Let Monkeys Eat Bananas

Passive immunity

- The short-term immunity that results from the introduction of antibodies from another person, location, animal, transferred or passed to us, can be acquired (think of mom giving colostrum to baby), still acquired but still passive

- An adaptive/acquired immunity

- B lymphocytes/T lymphocytes

Innate immunity

- Immunity we are born with, "In our Nature" In-nate

- Involves inflammatory process

- Neutrophils, Dendritic cells, Natural killer cells, Monocytes (that mature into macrophages)

- Neutrophils and Macrophages- Phagocytosis

- Natural killer cells- Non-specific cellular antigen destruction

- Dendritic cells- Antigen presentation

Active immunity

- A form of adaptive/acquired immunity in which the body produces its own antibodies against disease-causing antigens, uses energy

- B lymphocytes/T lymphocytes

Humoral immunity

- Adaptive immunity

- B lymphocytes: Antibodies secreted from plasma cells IgA, IgD, IgE, IgG, IgM and Memory cells

- Primary adaptive immune response (activation with first recognition of a specific antigen)

- Secondary adaptive immune response (reactivation with later recognition of the same antigen)

Cell-mediated immunity

- Adaptive Immunity

- Cytotoxic T lymphocytes: CD8

- Helper T lymphocytes (TH1, TH2): CD4

- Major histocompatibility complex (MHC): MHC class 1 molecules (CD8), MHC class 2 molecules (CD4), (Also known as human leukocyte antigen (HLA))

Alterations in immune function

- Host defense failure

- Hypersensitivity

- Autoimmunity

- Alloimmunity

- Examples include acquired immunodeficiency syndrome (AIDS), anaphylactic reaction, systemic lupus erythematosus (SLE)

Anaphylactic Reaction

- Exaggerated systemic immune response due to a type 1 hypersensitivity reaction, often triggered by things like insect stings, food allergies, and drug allergies

- Antigen exposure stimulates an IgE-mediated response in a previously sensitized individual.

- Degranulation of mast cells and basophils causes local and systemic responses such as dilation of vascular smooth muscle, constriction of bronchial smooth muscle, increase in vascular permeability

- Comes in 2 phases: (Phase 1)-Difficulty breathing, skin flushing/itching, and angioedema, (Phase 2)-Difficulty breathing, severe hypotension, severe edema

- Emergent treatment includes administering ephinephrine, diphenhydramine (Benadryl), and/or solumedrol

Preventative measures include desensitization to the problematic allergen

Host defense failure

- Antigenic variation

- Viral latency

- Immunodeficiency

Hypersensitivity

- Type 1 (immediate) hypersensitivity reaction

- Type II antibody-mediated hypersensitivity reaction

- Type III immune complex-mediated reaction (Systemic Lupus Erythymatosis)

- Type IV cytotoxic T lymphocyte-mediated hypersensitivity reaction: Direct cell-mediated toxicity, delayed hypersensitivity reaction

Systemic Lupus Erythmatosus

- Type III hypersensitivity reaction

- Autoimmune response

- Involves responses by the innate and adaptive immune systems

- Chronic disease due to persistent antigen, triggers activation of B cells, producing antibodies and activation of T cells, promoting inflammation

- Systemic condition: Autoantibodies targeted against the cell membrane, cytoplasm, and nucleus

- Clinical Manifestations: Specific to organs injured by inflammation and complex deposition, local, skin, musculoskeletal, pulmonary, and kidney, butterfly rash on face, systemic, neurologic, pulmonary, hematologic, and cardiac disease, joint pain, fatigue

Autoimmunity

The body attacks itself

Lymphatics

- Important in establishing the immune response (produces and stores immune cells, one of the methods of transport for immune cells, filters and removes pathogens, activates some immune responses and is a part of developing immune memory)

Infection

- A state of cellular, tissue, and organ destruction resulting from invasion by microorganisms

- Penetration of three lines of defense

- Multiple drug-resistant microbes

- Globalization and spread of harmful microbes

- Chain of Infection: Transmission, Entry, Susceptible Host, Infectious Agent, Reservoir, Exit, (Repeat Cycle)

- Five Stages: Incubation (pathogen entry), prodromal (mild, non-specific symptoms), illness (specific, peak symptoms), decline (symptoms fade), and convalescence (recovery)

-Complications can include septicemia, bacteremia, septic shock, and chronic infection

Manifestations

- Local: Heat, incapacitation, pain, edema, redness, lymphadenitis, purulent exudate

- Systemic: Fever, weakness, headache, malaise (feeling "off"), anorexia, nausea

Diagnostic tests and labs for infection

- White blood cell count (Leukocytosis, Leukopenia)

- Serum antibody levels

- Cultures

- Sensitivities

Exposure

Host exposed

Incubation

Time between exposure and the illness

Prodrome

The time between the earliest non-specific symptoms and the full, characteristic symptoms

Acute clinical illness

Sudden Onset and Last a Short Time

Potassium concept map and hypo/hyperkalemia

- K+

- Acceptable extracellular range is 3.5-5 mEq/L

- Acceptable intracellular range is 140-150 mEq/L

- Hypo/Hyperkalemia

- Electrolyte imbalances of Sodium, Calcium, and Potassium can also cause Hypo/Hypermagnesemia

- Hypokalemia (low potassium) often accompanies low phosphate levels

Antioncogenes

-tumor suppressor genes

-encode proteins that inhibit the cell cycle or participate in DNA repair processes

-mutation in these genes result in the loss of supression activity and thereby promote cancer

-inactivation of both alleles is necessary for the loss of 

function, therefore multiple mutations are required

Hormones and Cancer

- Some hormones can help in the treatment of some cancers, but some hormones can make other cancers worse

Mitosis

- a fundamental process of cell division where one parent cell divides to produce two genetically identical daughter cells (prophase, metaphase, anaphase, telophase, and cytokinesis)

Meiosis

- a two-stage cell division process that reduces a diploid cell into four haploid daughter cells, known as gametes

Osteoarthritis

 Damage to the joint through trauma or repetitive use, and then inflammation and arthritis occurs

Rheumatoid arthritis

- Often Bilateral

- Autoimmune disorder

- The immune system mistakenly attacks the synovium joint lining (membranes and hyperplasia) causing inflammation and arthritis

- Remissions: When the Person is Feeling Better

- Cartilage erosion

- Ankylosis: Fibrosis impairs joint mobility and can result in a debilitating fixation of the joint

- Pannus is granulation tissue that forms over the inflamed synovium and cartilage as a result of accelerated angiogenesis

Phagocytosis

- Form of endocytosis where cells, primarily immune cells like macrophages and neutrophils, bind to, engulf, and destroy large particles like bacteria, dead tissue, or foreign debris

Abcess

Pocket of purulent (containing pus) exudate

Chronic gastritis

chronic inflammation of stomach mucosa

Acute gastritis

Inflammation in the gastric mucosa most often caused by the ingestion of irritants such as aspirin, alcohol, or certain microorganisms

- Clinical Manifestations can include abdominal pain, indigestion, heart burn, nausea, vomiting, hiccups, or hematemesis. Anemia may result from mild gastric hemorrhage. Severe hemorrhage and perforation is quickly followed by shock and is a medical emergency.

- Diagnostic Criteria includes review of aspirin use in patient history, along with review of nonsteroidal anti-inflammatory drug use, excessive alcohol intake, recent contaminated food intake, or conditions causing ischemia of the gastric mucosa. The physical examination may reveal abdominal tenderness. May need stool sample to assess for internal bleeding/blood in the stool

- Treatment: Involves removal of the gastric irritant. Medications are then needed temporarily to buffer gastric acid or decrease gastric acid production. Gastritis and gastric ulceration healing depend on regeneration of the epithelial cells that line the gastric mucosa.

Acute phase reactants

Plasma proteins that act as inflammation markers

Acute pancreatitis

May occur when there is an injury to the acinar cells, pancreatic duct, or protective digestive feedback mechanisms in the exocrine pancreas. Common causes include duct blockage by gallstones or excessive alcohol use

Acute sinusitis

Inflammation of the lining of the paranasal sinuses lasting 4 to 8 weeks. Subacute sinusitis lasts 8 to 12 weeks. Recurrent acute sinusitis occurs when the patient has up to four episodes per year, with the sinus inflammation resolving completely between episodes

Adhesions

Fibrous connections between serous cavities and nearby tissues, which do not allow the surrounding tissues to move freely

Acute inflammation

- Typically resolves within a few weeks

- Minimal scarring 

- Neutrophils are the chief phagocytic cell 

- Goals of this inflammation are to increase blood flow to site of injury, prepare for tissue repair (Remove Injured Tissue), and to increase healing cells at site

Chronic inflammation

- Present for a prolonged period, usually greater than 6 months

- Monocytes, macrophages, and lymphocytes are the main WBCs/chief phagocytic cells

- Marked by fibrosis , scarring, or granuloma formation

Monocytes

Circulate in the blood to the site of injury and mature into macrophages in the tissues

Proteinases

- Enzymes that destroy elastin and other tissue components

- Acts to destroy dead tissue at the site of injury but can continue acting beyond that, and can destroy healthy new tissue as well

Fibroblasts

- Active in chronic inflammation

- Responsible for collagen development, which contributes to the extensive scarring characteristic of chronic inflammation

Scarring

Leads to permanent loss of the function and deformity of the tissue or organ

Granulomas

- Nodular inflammatory lesions that encase harmful substances

- Regulated by macrophages

- Typically form when the injury is too difficult to control by the usual inflammatory and immune mechanisms, such as with foreign bodies or certain microorganisms

Inflammatory vascular response

1) blood vessel dilation 

2) increased vascular permeability--> leakage

3) WBCs adhere to inner walls of vessels 

4) WBCs migrate through vessels (diapedesis)

Burn severity

correlated with exposure type and time

Classification of burns

- Superficial partial-thickness

- Deep partial-thickness

- Full-thickness

Superficial partial-thickness burns

Heat, swelling, pain, redness (erythema), loss of function

Deep partial-thickness burns

Blistering, redness, heat, pain, edema, serous exudate

Full-thickness burns

Redness, eschar, edema, exudate

Burns diagnostic criteria

- Wound depth, surface area, required level of treatment

Burns treatment

- Remove source of injury and cool/rinse skin

- Airway, breathing, circulation

- Fluids, nutrition, antibiotics, analgesics

- Wound management may include hydrotherapy or skin grafting

Rheumatoid Arthritis diagnostic criteria

Increased likelihood of

- Erythrocyte sedimentation rate (ESR)

- C-reactive protein (CRP)

- Rheumatoid factor (IgG)

- Antinuclear antibodies (ANA)

No definitive testing

Crohn’s disease

- Chronic autoimmune disorder that can occur anywhere in the digestive tract; however, it is most often found in the small intestine

- Clinical manifestations include abdominal pain, diarrhea, malnutrition, occult blood in stool, fever, weight loss and fatigue

- Diagnostic criteria includes history and physical examination, endoscopic examination, radiographs, computed tomography scans and stool cultures/samples

- Treatment includes symptom management, meds, dietary changes, and surgery

Ulcerative colitis

- Chronic inflammation begins in rectum and ascends the descending colon. Often presents as continuous superficial areas of ulceration.

- Perforation, obstruction, and massive hemorrhage can result.

- Signs/Symptoms can include diarrhea, rectal bleeding, abdominal pain, fever, weakness, fatigue, and anemia

- Diagnostic Criteria includes history and physical examination, endoscopic examination, radiographs, and labs/complete blood count (anemia)

- Treatments include management of symptoms, diet changes, surgery, and medication

Pressure ulcers

- Skin breakdown due to prolonged pressure

- Can come in 4 stages

Stage 1 of pressure ulcer or sore

- Non-blanchable inflamed area, intact skin with a localized area of redness. Can be painful, firm, soft, warmer, or cooler than surrounding skin.

Stage 2 of pressure ulcer or sore

- (Partial thickness skin loss): Open but shallow wound with a red-pink wound bed, typically without slough (dead tissue). It may also appear as an intact or ruptured serum-filled blister.

Stage 3 of pressure ulcer or sore

- (Full-thickness skin loss): A deep crater-like wound that extends into the subcutaneous tissue (fat) but does not expose muscle, tendon, or bone. Slough may be present, and undermining/tunneling might occur.

Stage 4 of pressure ulcer or sore

- (Full-thickness tissue loss): A severe, deep wound extending to the underlying muscle, tendon, or bone. Slough or eschar (black/brown dead tissue) is often present, and the wound often includes undermining or tunneling.

Erythema

Abnormal skin redness/inflammation

Eschar

a thick layer of dead tissue and tissue fluid that develops over a deep burn or other area of injury, such as a pressure sore/ulcer