Pathophysiology Final-Harper college/Horeni
What are the signs of fluid imbalance? ANSWER- Hypovolemia: dry mouth, cool feet, decrease
capillary refill, BP, increase pulse, serum osmo, albumin, urea; Hypervolemia:coughing, edema,
wheezing, increased BP, resp rate, and frothy sputum
What is hyponatremia? ANSWER- Low-sodium in blood less than 136meq/L; Signs include
anorexia, nausea and vomiting, weakness, restlessness, poor skin turgor, delirium,sucken eyes,
dry tongue, convulsions; Caused by diuretics, GI loss, renal dx; Labs: decreased urine spg
gravity
What is hypernatremia? ANSWER- Increased sodium Level > 145meq/L; Signs include
irritability, agitation, thirst, confusion, decreased urine output, twitching, seizures; R/T Increased
intake of sodium; Labs: increased serum osmo and urine sp. Gravity
What is hypokalemia? ANSWER- Decrease in potassium Level < 3.5 meq/L; Signs include
weakness, muscle irritability, confusion, nausea and vomiting, Cardiac dysrhythmias
,paresthesias, shallow respirations increased urine output, elevated serum pH (alkalosis); R/T
diuretic use, diarrhea, vomiting; Treatments includes potassium supplements and foods high
potassium
What is hyperkalemia? ANSWER- Increase in potassium > 5.0 meq/L; Signs include nausea or
vomiting and diarrhea, muscle cramps, weakness, arrhythmias, decreased serum pH (acidosis)
and urine output; R/T chronic renal failure, burns, acidosis and adrenal insufficiency; Treatment
includes Kay exalate and insulin.
What helps maintain oncotic pressure? ANSWER- It is maintained by plasma proteins
What is hypermagnesia? ANSWER- Magnesium level > 2.5 meq/L; Caused by CRF or excess of
intake of magnesium; Hemolyzed blood causes false increase of magnesium level; Delayed in
muscle activity
What would be observed upon assessment of a patient with hypermagnesia? ANSWER- Muscle
weakness, Decrease deep tendon reflex, Nausea and vomiting, Decreased respirations, Arrest
How would hypermagnesia be managed? ANSWER- Cardiac monitoring, Administer calcium
gluconate to rid Mg, Hydration, Monitor vital signs for decrease BP and respirations
What is hypomagnesia? ANSWER- Serum level < 1.5meq/L or 1.8mg/dl; Causes: inadequate
intake from alcoholism, bowel disease, excessive loss from gastric drainage; Occurs with renal
disease or endocrine disorders
What would be observed upon assessment of a patient with hypomagnesia? ANSWER- Increase
neuromuscular irritability, tremor, twitching, leg cramps, spasms and tetany; Mental
,disturbances, disorientation, restlessness; Hyperflexia; Cardiac arrhythmias and EKG changes;
Swallowing difficulty; Nausea and vomiting; Paralytic ileus; Positive Chvostek sign: spasm of
facial muscle inverted by the facial nerve when tapped; Positive Trousseau's sign ( carpal
spasms) causing contraction of fingers and hand when circulation is constructed one to four
minutes by BP cuff.
What is hypercalcemia? ANSWER- Calcium Level > 11 mg/dl; Increased absorption from
vitamin D; Endocrine disorder: hyperparathyroidism or adrenal insufficiency; Malignant disease
such as lymphoma, multiple myeloma, parathyroid tumors or bone metastasis; Conditions such
as osteoporosis, multiple fractures and immobilization increase calcium
What would be observed upon assessment of a patient with hypercalcemia? ANSWER-
Anorexia, nausea and vomiting; Constipation; Paralytic ileus; Confusion, weakness, and
lethargy; Blurred vision; Bone pain; Cardiac arrhythmias or arrest
How would hypercalcemia be managed? ANSWER- Increase the urinary excretion of calcium;
IV fluid and diuretics; Administer drugs to prevent calcium release from bone such as
pamidronate; Administer IV calcitonin to decrease reabsorption and increase urine excretion;
Monitor neurological status every four hours; Assess bone pain and medicate; Treat nausea and
vomiting
What is hypocalcemia? ANSWER- Serum Level < 8.5 mg/dl; Causes include chronic renal
failure, decrease absorption or intake of calcium malabsorption of calcium with GI diseases, and
vitamin D deficiency; Other causes are poor nutrition from alcoholism, excess of diarrhea, and
aggressive diuretic therapy; Low magnesium level decreases parathyroid secretion causing low
calcium
What would be observed upon assessment of a patient with hypocalcemia? ANSWER- Cramps,
muscle spasms, tetany; Laryngeal spasm; Convulsions; Parasthesis thesis of lips and extremities;
Positive Chvostek's and Trousseau sign; Arrhythmias, hearts block, and V-fib; Assess for
increased peristalsis and diarrhea; Osteoporosis
How would hypocalcemia be managed? ANSWER- In an emergency administer calcium
gluconate by IVP; Monitor calcium levels every six hours; Monitor IV site since calcium causes
tissue damage; If non-emergent administer oral calcium such as calcium carbonate tablets
What is respiratory acidosis? ANSWER- Increase CO2 creates carbonic acid; Airway
obstruction causes increase CO2 retention; Decrease brainstem stimulation with head injury
causes CO2 retention; Sedative overdose, narcotic in postop period
What is metabolic acidosis? ANSWER- Increase acid or decrease in base; Causes: Increase
hydrogen + from ketoacidosis, fever, hypoxia, Decrease hydrogen + elimination from chronic
renal disease, Decrease production of bicarbonate from renal failure or liver failure, Increase
elimination of bicarbonate with diarrhea or vomiting, Increased breakdown of fatty acids with
exercise increases pH, Seizures or hypermetabolic states such as ketoacidosis caused by diabetes,
Ingestion of acid substances such as aspirin, Renal failure causes acidosis since renal tubules
, cannot secrete hydrogen into urine, Decreased production of bicarbonate made in tubules and
pancreas because of diseases, Diarrhea- loss of intestinal and pancreatic fluids
What is respiratory alkalosis? ANSWER- Excess loss of CO2 from increase respiration rates;
R/T fever, anxiety, fear or improper ventilation settings, head injury, ASA poisoning
What is metabolic alkalosis? ANSWER- Increase in base or decrease in acid; R/T ingestion of
bicarbonate, acetates, citrates, or lactates from antibiotics, blood transfusions, TPN and treatment
of ketoacidosis; Loss of acid results from vomiting, NG suction or adrenal tumors;
Cardiovascular signs include increased heart rate, hypovolemia, decreased blood pressure and
decreased K+, CNS signs include agitation, confusion, tingling of mouth toes, seizures are hyper
reflexes, Muscular system includes cramps, spasm, decrease hand grip
Metabolic Acidosis ABG ANSWER- pH <7.35, PaCO2 normal, HCO3 <24 meq
Respiratory acidosis ABG ANSWER- pH < 7.35, PaCO2 > 45mmhg, HCO3 normal
Metabolic alkalosis ABG ANSWER- pH > 7.45, PaCO2 normal, HCO3 > 28meq
Respiratory alkalosis ABG ANSWER- pH > 7.45, PaCO2 < 35mmhg, HCO3 normal
What does hyperventilation do? ANSWER- decrease the amount of carbonic acid by blowing off
carbon dioxide and leaving water
What are the causes of infection? ANSWER- Bacteria, viruses, and/or fungi
What is Type 1 hypersensitivity? ANSWER- IgE mediated; Production of IgE antibody in
response to exposure to specific exogenous antigens; Against environmental antigens (allergens);
IgE binds to Fc receptors on surface of mast cells (cytotropic antibody); Histamine release;
Allergic reaction
What are the manifestations of type 1 hypersensitivities? ANSWER- Itching, Urticaria,
Conjunctivitis, Rhinitis, Hypotension, Bronchospasm, Dysrhythmias, GI cramps and
malabsorption
What are the treatments for type 1 hypersensitivities? ANSWER- Antihistamines, Anti-
inflammatories (e.g., inhaled corticosteroids, nasal steroids, prednisone), Bronchodilators, Anti-
leukotrienes, Anti-IgE antibody, Desensitization (allergy shots; immunotherapy),Epinephrine
(use is restricted to acute allergic reactions such as anaphylaxis)
What is type 2 hypersensitivity? ANSWER- Cell is destroyed by antibodies (IgG, IgM) and
complement. Antibody or complement attaches to cell and destroys; Cell destruction through
phagocytosis by macrophages; Antibody-dependent cell-mediated cytotoxicity. NK cells
recognize antibodies on target cell and cause target cell malfunction; Autoimmune hemolytic
anemia, hemolytic disease of the newborn, Goodpasture disease
What are the signs of fluid imbalance? ANSWER- Hypovolemia: dry mouth, cool feet, decrease
capillary refill, BP, increase pulse, serum osmo, albumin, urea; Hypervolemia:coughing, edema,
wheezing, increased BP, resp rate, and frothy sputum
What is hyponatremia? ANSWER- Low-sodium in blood less than 136meq/L; Signs include
anorexia, nausea and vomiting, weakness, restlessness, poor skin turgor, delirium,sucken eyes,
dry tongue, convulsions; Caused by diuretics, GI loss, renal dx; Labs: decreased urine spg
gravity
What is hypernatremia? ANSWER- Increased sodium Level > 145meq/L; Signs include
irritability, agitation, thirst, confusion, decreased urine output, twitching, seizures; R/T Increased
intake of sodium; Labs: increased serum osmo and urine sp. Gravity
What is hypokalemia? ANSWER- Decrease in potassium Level < 3.5 meq/L; Signs include
weakness, muscle irritability, confusion, nausea and vomiting, Cardiac dysrhythmias
,paresthesias, shallow respirations increased urine output, elevated serum pH (alkalosis); R/T
diuretic use, diarrhea, vomiting; Treatments includes potassium supplements and foods high
potassium
What is hyperkalemia? ANSWER- Increase in potassium > 5.0 meq/L; Signs include nausea or
vomiting and diarrhea, muscle cramps, weakness, arrhythmias, decreased serum pH (acidosis)
and urine output; R/T chronic renal failure, burns, acidosis and adrenal insufficiency; Treatment
includes Kay exalate and insulin.
What helps maintain oncotic pressure? ANSWER- It is maintained by plasma proteins
What is hypermagnesia? ANSWER- Magnesium level > 2.5 meq/L; Caused by CRF or excess of
intake of magnesium; Hemolyzed blood causes false increase of magnesium level; Delayed in
muscle activity
What would be observed upon assessment of a patient with hypermagnesia? ANSWER- Muscle
weakness, Decrease deep tendon reflex, Nausea and vomiting, Decreased respirations, Arrest
How would hypermagnesia be managed? ANSWER- Cardiac monitoring, Administer calcium
gluconate to rid Mg, Hydration, Monitor vital signs for decrease BP and respirations
What is hypomagnesia? ANSWER- Serum level < 1.5meq/L or 1.8mg/dl; Causes: inadequate
intake from alcoholism, bowel disease, excessive loss from gastric drainage; Occurs with renal
disease or endocrine disorders
What would be observed upon assessment of a patient with hypomagnesia? ANSWER- Increase
neuromuscular irritability, tremor, twitching, leg cramps, spasms and tetany; Mental
,disturbances, disorientation, restlessness; Hyperflexia; Cardiac arrhythmias and EKG changes;
Swallowing difficulty; Nausea and vomiting; Paralytic ileus; Positive Chvostek sign: spasm of
facial muscle inverted by the facial nerve when tapped; Positive Trousseau's sign ( carpal
spasms) causing contraction of fingers and hand when circulation is constructed one to four
minutes by BP cuff.
What is hypercalcemia? ANSWER- Calcium Level > 11 mg/dl; Increased absorption from
vitamin D; Endocrine disorder: hyperparathyroidism or adrenal insufficiency; Malignant disease
such as lymphoma, multiple myeloma, parathyroid tumors or bone metastasis; Conditions such
as osteoporosis, multiple fractures and immobilization increase calcium
What would be observed upon assessment of a patient with hypercalcemia? ANSWER-
Anorexia, nausea and vomiting; Constipation; Paralytic ileus; Confusion, weakness, and
lethargy; Blurred vision; Bone pain; Cardiac arrhythmias or arrest
How would hypercalcemia be managed? ANSWER- Increase the urinary excretion of calcium;
IV fluid and diuretics; Administer drugs to prevent calcium release from bone such as
pamidronate; Administer IV calcitonin to decrease reabsorption and increase urine excretion;
Monitor neurological status every four hours; Assess bone pain and medicate; Treat nausea and
vomiting
What is hypocalcemia? ANSWER- Serum Level < 8.5 mg/dl; Causes include chronic renal
failure, decrease absorption or intake of calcium malabsorption of calcium with GI diseases, and
vitamin D deficiency; Other causes are poor nutrition from alcoholism, excess of diarrhea, and
aggressive diuretic therapy; Low magnesium level decreases parathyroid secretion causing low
calcium
What would be observed upon assessment of a patient with hypocalcemia? ANSWER- Cramps,
muscle spasms, tetany; Laryngeal spasm; Convulsions; Parasthesis thesis of lips and extremities;
Positive Chvostek's and Trousseau sign; Arrhythmias, hearts block, and V-fib; Assess for
increased peristalsis and diarrhea; Osteoporosis
How would hypocalcemia be managed? ANSWER- In an emergency administer calcium
gluconate by IVP; Monitor calcium levels every six hours; Monitor IV site since calcium causes
tissue damage; If non-emergent administer oral calcium such as calcium carbonate tablets
What is respiratory acidosis? ANSWER- Increase CO2 creates carbonic acid; Airway
obstruction causes increase CO2 retention; Decrease brainstem stimulation with head injury
causes CO2 retention; Sedative overdose, narcotic in postop period
What is metabolic acidosis? ANSWER- Increase acid or decrease in base; Causes: Increase
hydrogen + from ketoacidosis, fever, hypoxia, Decrease hydrogen + elimination from chronic
renal disease, Decrease production of bicarbonate from renal failure or liver failure, Increase
elimination of bicarbonate with diarrhea or vomiting, Increased breakdown of fatty acids with
exercise increases pH, Seizures or hypermetabolic states such as ketoacidosis caused by diabetes,
Ingestion of acid substances such as aspirin, Renal failure causes acidosis since renal tubules
, cannot secrete hydrogen into urine, Decreased production of bicarbonate made in tubules and
pancreas because of diseases, Diarrhea- loss of intestinal and pancreatic fluids
What is respiratory alkalosis? ANSWER- Excess loss of CO2 from increase respiration rates;
R/T fever, anxiety, fear or improper ventilation settings, head injury, ASA poisoning
What is metabolic alkalosis? ANSWER- Increase in base or decrease in acid; R/T ingestion of
bicarbonate, acetates, citrates, or lactates from antibiotics, blood transfusions, TPN and treatment
of ketoacidosis; Loss of acid results from vomiting, NG suction or adrenal tumors;
Cardiovascular signs include increased heart rate, hypovolemia, decreased blood pressure and
decreased K+, CNS signs include agitation, confusion, tingling of mouth toes, seizures are hyper
reflexes, Muscular system includes cramps, spasm, decrease hand grip
Metabolic Acidosis ABG ANSWER- pH <7.35, PaCO2 normal, HCO3 <24 meq
Respiratory acidosis ABG ANSWER- pH < 7.35, PaCO2 > 45mmhg, HCO3 normal
Metabolic alkalosis ABG ANSWER- pH > 7.45, PaCO2 normal, HCO3 > 28meq
Respiratory alkalosis ABG ANSWER- pH > 7.45, PaCO2 < 35mmhg, HCO3 normal
What does hyperventilation do? ANSWER- decrease the amount of carbonic acid by blowing off
carbon dioxide and leaving water
What are the causes of infection? ANSWER- Bacteria, viruses, and/or fungi
What is Type 1 hypersensitivity? ANSWER- IgE mediated; Production of IgE antibody in
response to exposure to specific exogenous antigens; Against environmental antigens (allergens);
IgE binds to Fc receptors on surface of mast cells (cytotropic antibody); Histamine release;
Allergic reaction
What are the manifestations of type 1 hypersensitivities? ANSWER- Itching, Urticaria,
Conjunctivitis, Rhinitis, Hypotension, Bronchospasm, Dysrhythmias, GI cramps and
malabsorption
What are the treatments for type 1 hypersensitivities? ANSWER- Antihistamines, Anti-
inflammatories (e.g., inhaled corticosteroids, nasal steroids, prednisone), Bronchodilators, Anti-
leukotrienes, Anti-IgE antibody, Desensitization (allergy shots; immunotherapy),Epinephrine
(use is restricted to acute allergic reactions such as anaphylaxis)
What is type 2 hypersensitivity? ANSWER- Cell is destroyed by antibodies (IgG, IgM) and
complement. Antibody or complement attaches to cell and destroys; Cell destruction through
phagocytosis by macrophages; Antibody-dependent cell-mediated cytotoxicity. NK cells
recognize antibodies on target cell and cause target cell malfunction; Autoimmune hemolytic
anemia, hemolytic disease of the newborn, Goodpasture disease
