Pathophysiology
When exposed to adverse conditions, cells undergo a process to protect themselves
Atrophy- Decreased in cell size
Hypertrophy- increase in cell size
hyperplasia- increase in cell number
Dysplasia- Alteration in cell size, shape, and organization
Metaplasia- Cell type is replaced by another
Disturbances in fluid balance
-The human body is mostly water
all biochemical reactions in the body occur in a aqueous environment
-Degree of fluid imbalnce required to compromise homeostasis and cause illness depends on the patients’s—
Size
Age
underlying medical conditions
Edema
Excessive amounts of fluid in the interstitial space
causes are:
Increased capillary tissue
decreased colloidal osmotic pressure
lymphatic vessel obstruction
Isotonic fluid deficit and excess
deficit- Decrease in extracellular fluid with proportionate losses of sodium and water
excess- Increase in extracellular fluid with proportionate increases in both sodium and water
Sodium
Normal levels: 136-142 mEq/L
Hypertonic fluid deficit: Caused by excess water loss without proportinate loss of sodium
Hypotonic fluid deficit- caused by excess sodium loss with less water loss
hyponatremia- low salt in the blood. less than 136 mEq/L
Hypernatremia- High salt in the blood. over 142 mEq/L
Potassium
Normal levels: 3.5 to 5.0 mEq/L
Hypokalemia-low calcium levels in the blood. can lead to cardiac arrythmias
Hyperkalemia- High potassium in the blood. Often found in dialysis pts. can lead to cardiac arrythmias
Calcium
Normal levels: 8.2 - 10.2 mEq/L
Hypocalcemia- Decreased serum calcium levels
Hypercalcemia- increased serum calcium level
Phosphate
Normal levels- 2.3 - 4.7 mg/dL
Hypophosphatemia- low phosphate. leads to feeling lathargic
Hyperphosphatemia- increased phosphate level
Magnesium
Normal levels: 1.3 to 2.1 mg/dL
Hypomagnesemia- low magnesium
hypermagnesemia- High magnesium
Electrolyte Imbalances
Disturbances of Acid - base balance
The lower the pph the higher the acidity
acids and bases neutralize each other and must remained balanced
Fluctuations in ph due to bicarbonate level: metabolic acidosis or alkalosis. DKA is metabolic acidosis
Fluctuations in ph due to respiratory disorders: respiratory acidosis or alkalosis, low respiration rate will lead to acidosis high respirations will lead to alkalosis
a disorder not correctable by buffers initiates compensatory mechanisms
Respiratory acidosis
related to hypoventilation
COPD creats acidosis overtime
Compensatory machanism is the renal buffer system
Respiratory alkalosis
Associated with conditions that result in hyperventilation
Carbon dioxide levels in the blood drops
renal system retains H+ ions
Metabolic acidosis: Any acidosis not related to respiratory
causes could include:
lactic acidosis
ketoacidosis
GI losses
ingestion of drugs or toxins
Metabolic alkalosis: Occurs with excessive acid loss
causes include:
Excessive vomiting
excessive water intake
nasogastric suctioning
excessive intake of alkaline substances
Hypoxic Injury
Damage in individual cells often affects the entire organism
entire organ system may fail
repair may occur with proper treatment
irreversible injury will lead to cell death
cell death is followed by
Cells that are hypoxic for more than a few seconds will produce Mediators
-The earliest and most dangerous mediator is free radicals
chemical instability causes attacks on other cells and the cell membrane
Chemical Injury
Common poisons: cyanide and pesticides
Lead: long-term ingestion leads to brain injury and neurological dysfunction
Carbon monoxide: binds to hemoglobin and prevents adequate oxygenation of tissue
Ethanol: May result in CNS depression, hypoventilation, and cardiovascular collapse
Pharmacologic agents: produce toxic products when metabolized in the body
Infectious Injury
Virulence measures disease causing ability
Pathogenicity: Function of microorganisms ability to reproduce and cause diseases
Signs of Inflammation
Heat
Redness
tenderness
swelling
Pain
SIRS
Systemic
inflammatory
Response
System
local effects: Dialation of blood vessels and increased vascular permeability
cellular membranes ma be injured in process
Apoptosis
Normal cell death
cell exhibits characteristic nuclear changes and die in clusters
controlled degraadation allows their remnants to be taken up and reused
Necrosis
Result of morphologic changes following cell death
simple: gross and microscopic tissue a d cells are recognizeable
derived: caseation necrosis, dry gangrene, ft necrosis, liquefaction necrosis
Systemic effects: Temperature elevation and increased leukocytes
Hypoperfusion
Response:
release of catecholamines
activation of renin-angiostensin- aldosterone system(RAAS)
release of antidiuretic hormone
fluid shifts from interstitial tissues to vascular compartment
Overall response: increased preload, stroke volume, heart rate
Immune response
Primary response- takes place during the first exposure to an antigen
secondary response- occurs with repeat exposure to an antigen
Antibody: Binds to antigen so the complex can attach itself to immune cells that destroy the complex
Immunogen: Antigen that is capable of starting a immune response
Humoral immune response
T-lymphocytes creates cell mediated immunity
B-lymphocytes create humoral immunity
Both make memory cells
Immunoglobins: antibodies secreated by b cells
three main antigens on antibodies
Isotypic:
igg is the most common immunoglobulin
igm
ige
table 9.4
Cell mediated immune response
Characterised by formation of lymphocytes
T cells lymphocytes recognize antigens by:
secreting cytokines
Becoming cytotoxic and killing abnormal cells
Killer T cells
helper t cells
memory t cells:
Acute inflamationb
involved both vascular and celluler componments
Kallikrenin; enzyme found in blood plasma, urine, and tissue
Bradykinin
Hagemen