Clinical Pathophysiology Final Study Guide

Atrophy

Cells decrease in size because demand decreases

Reversible

Etiologies of Atrophy

Disuse

Ischemia

Endocrine dysfunction

Persistent cell injury

Aging

Hypertrophy

Cells increase in size because of increased demand

Physiologic Etiologies of Hypertrophy

Normal

Weightlifting

Pathologic Etiologies of Hypertrophy

Abnormal

Enlarged Organs

Hyperplasia

Increase in number of cells

Physiologic Etiologies of Hyperplasia

Breast and uterine enlargement during pregnancy

Pathologic Etiologies of Hyperplasia

Enlargement of the prostate gland.

Metaplasia

Replacement of one differentiated cell type with another

Cell retains same basic tissue type

Reversible

Etiologies of Metaplasia

Occurs in response to chronic irritation and inflammation

Dysplasia

Deranged cellular growth, cells mutate with abnormal variations in size, shape, and arrangement

Can be reversible if you remove the trigger

Dysplasia is a strong precursor to what?

Cancer

Most common cause of cellular injury is?

Hypoxia

Hypoxia

Lack of oxygen inside the cells

Hypoxia results from…

Reduced amount of oxygen in the air

Loss of hemoglobin or decreased efficacy of hemoglobin

Decreased production of red blood cells

Diseases of the respiratory and cardiovascular systems

Poisoning of the oxidative enzymes within the cells (carbon monoxide)

Most common cause of Hypoxia is?

Ischemia

Can be progressive or acute

The progressive cause of ischemia which causes hypoxic injury is?

Arteriosclerosis

The acute cause of ischemia which causes hypoxic injury is?

Thrombosis

Ischemia-Reperfusion Injury

Free radicals and reactive oxygen species

Additional injury can be caused by the restoration of blood flow and oxygen

Chemical Injury

Direct toxicity to the cell membrane or formation of free radicals.

Necrosis

Cell injury which results in the premature death of cells in living tissues by autolysis

Caused by factors external to the cell or tissue such as infection, toxins, and trauma

Apoptosis

The process of eliminating unwanted cells, called programmed cell death

Coagulative Necrosis

Interruption of blood flow

Etiologies of Coagulative Necrosis

Ischemia

Location of Coagulative Necrosis

Kidneys, heart, and adrenal glands

Liquefactive Necrosis

Ischemia of neurons and glial cells of the brain

Etiologies of Liquefactive Necrosis

Bacterial Infection

* Staphylococci
* Streptococci
* Escherichia Coli

Location of Liquefactive Necrosis

Neurons and glial cells of the brain

Caseous Necrosis

Combination of liquefactive and coagulative necrosis

Etiologies of Caseous Necrosis

TB infection

Location of Caseous Necrosis

Lungs

Etiologies of Fat Necrosis

Action of lipases

Location of Fat Necrosis

Breast, pancreas, and other abdominal organs

Gangrenous Necrosis

Death of tissue from severe hypoxic injury

Etiologies of Gangrenous Necrosis

Severe hypoxic injury

Location of Gangrenous Necrosis

Wet: Feet and toes

Dry: Toes

Gas (Clostridium): Thigh

Somatic Death

Systemic death of an entire person

Algor Mortis

Postmortem reduction of body temperature

Livor Mortis

Purple discoloration from settling of blood in the most dependent tissues

Rigor Mortis

Stiffening develops within 12-14 hours and usually affects entire body

Gradually diminishes as the body becomes flaccid between 36-62 hours

GAS

General Adaptation Syndrome

Three stages: Alarm, Resistance, and Exhaustion

Alarm Stage

“Fight or Flight”

Stressors trigger hypothalamic-pituitary-adrenal (HPA) axis which activates sympathetic nervous system

Epinephrine, Norepinephrine, and Cortisol are released

Resistance Stage

Body attempts to restore homeostasis

Actions of adrenal hormones

Continued mobilization of the body’s resources to cope and overcome a sustained challenge

Exhaustion/Allosteric Overload Stage

Body can no longer produce hormones, Marks the onset of disease

Occurs only if the stress continues and adaptation is not successful

Body’s physiologic and immune systems no longer effectively cope with the stressor

Osmotic Pressure

Pulling pressure

Hydrostatic Pressure

Pushing pressure

Edema

Excessive accumulation of fluid within the interstitial spaces

Etiologies of Edema: Increased capillary hydrostatic pressure

Venous obstruction, salt and water retention, heart failure

Etiologies of Edema: Decrease in plasma oncotic pressure

Decreased synthesis of plasma proteins (cirrhosis, malnutrition)

Increased loss of plasma proteins (nephrotic syndrome)

Increased plasma Na+ and H2O retention (dilution of plasma proteins)

Etiologies of Edema: Increase in capillary permeability

Burns and inflammation

ADH

Tap water hormone

Causes kidneys to reabsorb water

Aldosterone

Saltwater hormone

Causes kidneys to reabsorb sodium and water

Etiologies of Fluid Volume Excess

Excessive sodium or water intake

Inadequate sodium or water elimination

Clinical Manifestations of Fluid Volume Excess

Generalized edema

Localized edema

Dyspnea

Bounding pulse

Tachycardia

Polyuria

Rapid weight gain

JVD

Crackles

Etiologies of Fluid Volume Deficit

Inadequate fluid intake

Excessive fluid or sodium loss

Clinical Manifestations of Fluid Volume Deficit

Thirst

Altered level of consciousness

Hypotension

Tachycardia

Weak, thready pulse

Flat jugular veins

Dry mucous membranes

Decreased skin turgor

Oliguria

Weight loss

Normal Sodium Values

136 - 145

Etiologies of Hyponatremia

Loss of sodium

Inadequate sodium intake

Sodium dilution from too much water

Clinical Manifestations of Hyponatremia

Lethargy

Confusion

Decreased reflexes

Muscle cramps and fatigue

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Complications of Hyponatremia

Cerebral edema

Increased intracranial pressure

Seizures

Coma

Etiologies of Hypernatremia

Inadequate water intake

Loss of water in ECF

Increased concentration of sodium in ECF

Clinical Manifestations of Hypernatremia

Thrist

Weight loss

Increased blood pressure

Muscle twitching

Increased reflexes

Complications of Hypernatremia

Coma

Convulsions

Cerebral Hemorrhage

Seizures

Normal Potassium Values

3\.5 - 5

Etiologies of Hypokalemia

Decreased intake

Increased entry of potassium into cell

Acid base balance

Increase in aldosterone

Insulin overuse

Increased loss of potassium

NG suctioning

Burns

Vomiting and diarrhea

Use of non potassium sparing diuretics

Clinical Manifestations of Hypokalemia

Neuromuscular excitability decreases

Skeletal muscle weakness

Loss of smooth muscle tone

Cardiac dysrhythmias

Prolonged PR interval

Flat T wave

Prominent U wave

Etiologies of Hyperkalemia

Increased intake

Potassium leaves the cells and goes into the blood

Decreased renal excretion of potassium

Insulin deficiency

Large infusion of stored blood

Cell trauma

Clinical Manifestations of Hyperkalemia

Neuromuscular excitability increases THEN decreases

Mild Attacks:

* Tingling of the lips and fingers
* Restlessness
* Tall, peaked T waves

Severe Attacks:

* Muscle weakness
* Loss of muscle tone
* Flaccid paralysis
* Cardiac dysrhythmias

Normal Calcium Values

9 - 10.5

Etiologies of Hypocalcemia

Insufficient dietary intake

Inadequate intestinal absorption

Blood administration

Renal Disease

Vitamin D Deficiency

Decreased in PTH

Clinical Manifestations of Hypocalcemia

Neuromuscular irritability (spasms, cramps)

Hyperactive reflexes

Tetany

Positive Trousseau sign

Positive Chvostek sign

Cardiac dysrhythmias

Etiologies of Hypercalcemia

Vitamin D overdose

Prolonged immobilization

Some cancers

Hyperparathyroidism

Clinical Manifestations of Hypercalcemia

Muscle weakness

Cardiac dysrhythmias (bradycardia, cardiac arrest)

Bone pain, osteoporosis

Pathological fractures

Impaired renal function

Kidney stones

Fatigue, weakness, lethargy, nausea, constipation

Normal Phosphate Values

3 - 4.5

Normal Magnesium Values

1\.3 - 2.1

Neutrophils

Predominate in early inflammatory responses, around 6-12 hours after initial injury

Ingest bacteria, dead cells, and cellular debris

Short lived and become a component of the purulent exudate

Eosinophils

Mildly phagocytic

Defense against parasites and regulation of vascular mediators

Basophils

Least prevelant

Primary role is unknown

Act like mast cells

Monocytes

Produced in the bone marrow, enter circulation, and migrate to the inflammatory site where they develop into macrophages

Macrophages

Typically arrive at the inflammatory site 24 hours or later after the neutrophils

Can live for months to years because they are capable of cellular division

Dendritic Cells

In peripheral organs and skin

Migrate through lymph vessels to lymph tissue and interact with T lymphocytes to generate an acquired immune response

Primary Intention Wound Healing

Wounds that heal under conditions of minimal tissue loss

Secondary Intention Wound Healing

Wounds that require a great deal more tissue replacement.

Ex: open wounds

Naturally Acquired Active Immunity

Exposure to antigen

Antigens enter the body naturally; body induces antibodies and specialized lymphocytes

Naturally Acquired Passive Immunity

Maternal antibodies in the mother’s breast milk (IgA) or antibodies that cross the placenta (IgG)

Artificially Acquired Active Immunity

Antigens introduced by vaccines

Antigens enter the body through vaccines; body produces antibodies and specialized lymphocytes

Artificially Acquired Passive Immunity

Preformed antibodies or T-cells are injected

Antibodies

Protect the individual from infection

Produced by B cells

IgG, IgA, IgM, IgE, and IgD

IgG

Most abundant (80-85%)

Accounts for most of the protective activity against infections

Transported across the placenta

Major antibacterial and antiviral antibody

IgA

IgA found predominately in the blood

IgA-2 found predominately in bodily secretions (most important)

Defends against pathogens on body surfaces, especially those that enter the respiratory and GI tracts

IgM

First antibody produced during the primary response to an antigen

Eliminates pathogens in the early stages of B-cell mediated immunity before there is sufficient IgG

IgD

Low concentration in the blood

Function as one type of B cell antigen receptor

Activates basophils and mast cells to produce antimicrobial factors

IgE

Mediator of many common allergic reactions

Defender against parasites

Stimulates the release of mast cell granules, which contain histamine and heparin

Hypersensitivity Type 1

IgE mediated

Genetic/hereditary in origin

Ex: Allergies, Hay Fever

Hypersensitivity Type 2

Tissue-specific reactions

Cell destruction by antibody and complement (ex blood transfusion)

Cell destruction through phagocytosis

Hypersensitivity Type 3

Immune complex mediated

Antibodies bind to soluble antigen that was released into the body or fluids, and then complex is deposited into tissues (ex gluten allergy, lupus)

Hypersensitivity Type 4

Does not involve antibodies at all

Cell mediated

Mediated by T lymphocytes (ex poison ivy, TB skin test)

Shunting

Perfusion without ventilation

Dead Space

Ventilation without perfusion

Hypoxemia

Abnormal low amount of O2 in the blood