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Pathophysiology Exams > Pathophysiology Exam I > Flashcards

Pathophysiology Exam I Flashcards

1
Q

Pathology

A

study of the change in body tissue and organs due to disease

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2
Q

Physiology

A

study of characteristics and function of a living organism

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3
Q

Pathophysiology

A

study of human physiologic function in disease; abnormal functioning of organs in disease

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4
Q

Symptom

A

a subjective indication of a disease or a change in condition as perceived by the client

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5
Q

Sign

A

an objective finding as perceived by the examiner

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6
Q

Etiology

A

cause of disease

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7
Q

Idiopathic

A

unknown cause

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8
Q

Homeostasis

A

main goal of the body, maintains stable equilibrium and regulates the body

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9
Q

three structures in the brain maintaining homeostasis

A
  1. medulla (respiratory and circulatory)
  2. pituitary gland (growth and reproduction
  3. reticular formation (brain stem)
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10
Q

Plasma Membrane

A
  • “bouncer” of the cell
  • controls the composition of the space or compartment they enclose
  • controls movement of substances from one cell to another
  • cellular mobility and maintenance of cellular shape
  • exert a powerful influence on metabolic pathways
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11
Q

structure of plasma membrane

A
  • cavolae – outer surface, serve as a storage site for receptors and provides route of transport into the cell
  • lipids – bilayer of basic components, serve as a barrier but allows transport of oxygen and carbon dioxide
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12
Q

function of plasma membrane

A
  • recognize and bind units
  • pores of transport channels
  • electrolytes and fluid balance
  • cell surfaces markers identify a cell to another
  • cell adhesion molecules that allow cells to join together and form attachments
  • catalyst of chemical reactions
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13
Q

Endocytosis

A

plasma membrane “taking in” – bringing food into the cell

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14
Q

Pinocytosis

A

ingestion of fluid – drink the fluid brought in by the endocytosis

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15
Q

Phagocytosis

A

ingestion of large particles – eat the food brought in by endocytosis

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16
Q

Exocytosis

A

release intracellular substances into extracellular matrix – kicks out extra substances

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17
Q

Passive Transport

A
  • small, uncharged molecules move easily through semipermeable membrane
  • driven by osmosis, hydrostatic pressure, and diffusion
  • DOES NOT REQUIRED ENERGY
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18
Q

Active Transport

A

Moving of large molecules requiring life, biologic activity and ENERGY

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19
Q

Diffusion

A

SOLUTES moves through a concentration gradient from an are of high concentration to an area of low concentration

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20
Q

Filtration

A

Movement of water and solutes through a membrane due to a pushing force on either side

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21
Q

Hydrostatic Pressure

A
  • mechanical force of water pushing against cellular membranes
  • PUSH PRESSURE
  • counteracted by oncotic pressure to maintain homeostasis
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22
Q

Osmosis

A

movement of WATER down a concentration gradient across a semi-permeable membrane from high water concentration to lower water concentration

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23
Q

Osmotic Pressure

A

amount of hydrostatic pressure required to oppose the osmotic movement of water

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24
Q

Oncotic pressure

A
  • PULL PRESSURE, opposes hydrostatic pressure
  • example: hydrostatic pressure pushes water out to the body (causes edema) and oncotic pressure keeps the water in the blood stream
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25
Q

Isotonic

A

osmolality is the same as intracellular fluid

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26
Q

hypertonic

A

osmolality is high than intracellular fluid (shrinks)

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27
Q

Hypotonic

A

osmolality is lower than intracellular fluid (swells)

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28
Q

Cellular atrophy

A
  • decrease in cellular size and function
  • causes: disuse, nerve damage, impaired nutrition, aging, diminished blood supply, lack of endocrine stimulation
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29
Q

Cellular hypertrophy

A
  • increased cellular size and function
  • causes = excessive use of tissue
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30
Q

Cellular hyperplasia

A
  • increased number of cells
  • cells are dividing faster than dying off
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31
Q

Hypoxia

A
  • single most common cause of cellular injury
  • results from: reduced amount of oxygen in air, loss of hemoglobin or decreased efficacy of hemoglobin, decreased production of RBCs, diseases of the respiratory and cardiovascular system
  • ischemia – most common cause of hypoxia
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32
Q

water accumulation

A
  • malfunction of Na+/K+ pump
  • cell swells with water
  • enlargement of organs
  • seen with almost all types of cellular injury
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33
Q

coagulative necrosis

A
  • tissue hypoxia
  • protein denature
  • occurs primarily in kidneys, heart and adrenal glands
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34
Q

liquiefactive necrosis

A
  • neurons and glial cells of the brain
  • cells auto digested
  • tissue liquefies and is walled off from healthy tissue
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35
Q

Caseous necrosis

A
  • tuberculous pulmonary infection
  • combination of coagulative and liquefactive necrosis
  • necrotic debris surrounded by the wall of tissue
  • “cheesy” debris
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36
Q

Fat necrosis

A
  • breakdown of triglycerides
  • occurs in breast, pancreas
  • appears chalky, white
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37
Q

dry gangrene

A

tissue shrinks, definitive line between dead and alive tissue

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38
Q

wet gangrene

A
  • cold, swollen tissue
  • foul odor
  • bacteria present
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39
Q

total body water

A
  • intracellular fluid = 2/3 of total body water
  • extracellular fluid = 1/3 of total body water
  • interstitial fluid = tissue, outside of cell and blood vessel
  • intravascular fluid – inside the blood vessel, outside the cell
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40
Q

capillary hydrostatic pressure

A

facilitates movement of water from capillary to interstitial space

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41
Q

capillary oncotic pressure

A

osmotically attracts water from interstitial back into capillary

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42
Q

interstitial hydrostatic pressure

A

facilitates inward movement of water from interstitial into capillary

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43
Q

interstitial oncotic pressure

A

osmotically attracts water from capillary into interstitial space

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44
Q

Atrial Natriuretic Peptide

A
  • hormone increases rate of excretion of Na+ in urine
  • hormone synthesized and stored in atrial muscle
  • receptors in atria are stimulated in response to increased blood volume
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45
Q

Edema

A
  • excessive accumulation of fluid within the interstitial spaces
  • related to fluid filtration from capillaries or lymph channels into tissues
  • causes = increase in capillary hydrostatic pressure, decrease in plasma oncotic pressure, increases in capillary permeability, lymph obstruction
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46
Q

localized edema

A

usually limited to a site of trauma to a site of trauma or within a particular organ system

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47
Q

generalized edema

A

more uniform distribution of fluid in interstitial space

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48
Q

Sodium, Chloride, and water balance

A
  • water balance is regulated primarily by antidiuretic hormone (made in pituitary, hold onto fluid) also known as vasopressin
  • secreted during low blood pressure or decrease in circulating blood volume
  • sodium is regulated by renal effects of aldosterone
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49
Q

stimuli for thirst

A
  • cellular dehydration – osmoreceptors
  • decreased blood volume - baroreceptors
  • angiotensin II
  • make them crave salt to increase thirst
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50
Q

Antidiuretic Hormone

A
  • holds onto fluid
  • vasoconstriction effect – increases BP
  • prevents excretion of water by kidneys
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51
Q

renal regulation

A
  • kidneys are the primary organs of fluid and electrolyte balance
  • water balance is maintained through urinary excretion
    renal tubules are stimulated by ADH and aldosterone to control the concentration of urine
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52
Q

RAAS

A
  • renin, agiotension, aldosterone system
  • purpose is to increase sodium and water reabsorption
  • can cause vasoconstriction to increase BP
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53
Q

isotonic alterations

A
  • occur when changes in total body water are accompanied by proportional changes in electrolytes
  • number of particle is equal on both sides of the membrane
  • fluid will not move in or out of cells
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54
Q

isotonic fluid loss

A
  • hemorrhage
  • severe wound drainage
  • excessive diaphoresis
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55
Q

isotonic fluid excess

A
  • excessive administration of IV normal saline
  • over excretion of aldosterone with renal retention
  • heart/renal failure
56
Q

clinical manifestations of isotonic alteration

A
  • loss = weight loss, dryness of skin, mucous membranes, hypotension, tachycardia, thirst
  • excess = weight, jugular vein distention, edema, pulmonary edema, hypertension
57
Q

hypotonic

A
  • a lower solute concentration
  • osmolality of ECF is less than normal
  • imbalance that results in an ECF less than 0.9% saline solution
  • hyponatremia decreases the ECF osmotic pressure, and water moves into the cells
  • normal sodium level = 135-145 mEq/L
58
Q

Hypotonic alterations – Hyponatremia

A
  • sodium causes movement of water into cells – causing cellular swelling
  • excessive loss = vomiting, diarrhea, GI suction, diuretics, lethargy, irritability, confusion, tachycardia, hypotension, seizures, tremors, decreased reflexes, coma
  • excessive gain = IV replacement, psychogenic polydipsia, heart failure, renal failure, headache, weakness, confusion, weight gain, hypertension, lethargy, decreased reflexes, seizures and coma
59
Q

hypertonic

A
  • a higher solute concentration
  • imbalance that results in ECF greater than 0.9% saline solution
  • osmolality of ECF is greater than normal
  • 3% saline solution – to get rid of cerebral edema
  • causes cellular shrinking
60
Q

hypertonic alterations

A
  • hypernatremia = water deficit
  • manifestation = symptoms of dehydration, tachycardia, weak pulses and postural hypotension, thirst (severe dehydration)
  • hyperchloremia = occurs with hypernatremia and bicarbonate deficit, managing by treating underlying disorder
  • clinical manifestations = nothing specific
61
Q

potassium

A
  • normal 3.5-5.0
  • 98% in the intracellular fluid
  • Na+/K+ pump maintains balance
62
Q

functions of potassium

A
  1. predominant ICF ion
  2. Maintains resting membrane potential
  3. required for deposit of glycogen in liver and skeletal muscle
  4. normal cardiac rhythms
  5. skeletal and smooth muscle contraction
63
Q

Potassium regulated by kidney

A
  • secreted into urine by distal tubule
  • reabsorbed by proximal tubule and loop of henle
64
Q

potassium regulated by aldosterone

A
  • when K+ concentration increases, aldosterone is released and stimulates K+ release into the urine via distal tubule
65
Q

potassium regulated by acid-base

A
  • in alkalosis, H+ moves into ECF and moves into cell = hypokalemia
  • in acidosis, H+ moves into cell and K+ moves into ECF = hyperkalemia
  • K+ exchange for H+ cation
66
Q

potassium regulated by insulin

A
  • secretion of insulin promotes movement of K+ into liver and muscle cells
  • insulin causes K+ shift into cells
  • used to treat hyperkalemia (increased blood sugar can contribute to hyperkalemia, ketoacidosis)
67
Q

Hypokalemia pathophysiology

A
  • decreased K+ in the ECF, indicates loss of total body K+ measured in ECF
  • total body K+ is depleted
  • K+ = <3.5mEq/L
68
Q

Hypokalemia causes

A
  • alkalosis = K+ shifts into the cell and H+ moves into the ECF to improve acid-base balance
  • insulin administration = when insulin is given, K+ moves to ICF and out of blood
  • decreased intake = poor nutrition
  • increased losses = GI losses, renal losses
69
Q

Hypokalemia clinical manifestations

A
  • muscular weakness and fatigue
  • cardiac dysrhythmias
  • anorexia, nausea, vomiting
  • depression and confusion
  • polyuria
70
Q

Hyperkalemia pathophysiology

A
  • increase Potassium in the ECF: indicated gain of total body K+ measured in ECF
  • total body K+ is excessive
  • K+ = >5.0 mEq/L
71
Q

Hyperkalemia causes

A
  • increased intake = K+ replacement therapy, whole blood transfusions, food
  • renal dysfunction or failure = most common, acute or chronic renal failure, kidneys are unable to excrete K+
  • Shift from ICF to ECF
  • hypoaldosteronism
72
Q

Hyperkalemia Clinical Manifestations

A
  • muscle weakness
  • muscle and intestinal cramping
  • nausea, vomiting, diarrhea
  • cardiac dysrhythmias
  • paresthesias
  • anxiety, restless
73
Q

Calcium and Phosphate

A
  • calcium and phosphate concentration are rigidly controlled
  • inverse relationship
74
Q

Calcium

A
  • necessary for structure of bones and teeth, blood clotting, hormone secretion, cell receptor function, plasma membrane stability, transmission of nerve impulses, muscle contraction
  • normal range = 8.6-10.2 mg/dL
75
Q

Hypocalcemia

A
  • causes = inadequate intestinal absorption, deposition of ionized calcium into bone or soft tissue, blood administration, decrease in PTH and vitamin D, nutritional deficiencies occur with inadequate sources of dairy products or vegetables
  • effects = increased neuromuscular excitability, convulsions and tetany, prolonged QT interval, cardiac arrest
76
Q

Hypercalcemia

A
  • causes = hyperparathyroidism, bone metastases with calcium reabsorption from breast, prostate, renal, and cervical cancer, sarcoidosis, excessive vitamin D, many tumors that produce PTH
  • effects = nonspecific, fatigue, lethargy, anorexia, nausea, constipation, impaired renal function, kidney stones, dysrhythmias, bradycardia, cardiac arrest, bone pain, osteoporosis
77
Q

Phosphate

A
  • located in the bone
  • necessary for high-energy bonds located in creatine phosphate and ATP and acts as an anion buffer
  • normal range 2.5 - 4.5
78
Q

hypophosphatemia

A
  • caused by = intestinal malabsorption, malabsorption syndromes, increased renal excretion of phosphate associated with hyperparathyroidism
  • effects = reduced capacity for oxygen transport for RBC, leukocyte and platelet dysfunction, deranged nerve and muscle function, irritability, confusion, numbness, coma, convulsions, possibly respiratory failure, cardiomyopathies
79
Q

Hyperphosphatemia

A
  • causes = acute or chronic renal failure with significant loss of glomerular filtration, treatment of metastatic tumors with chemotherapy, long term use of laxatives, hypoparathyroidism
  • effects = symptoms primarily related to low calcium levels, when prolonged, calcification of soft tissues in lungs, kidneys, joints
80
Q

Magnesium

A
  • intracellular cation
  • normal range 1.6-2.6
  • acts as a cofactor in intracellular enzymatic reactions
  • increases neuromuscular excitability
81
Q

Hypomagnesemia

A
  • causes = malnutrition, malabsorption syndrome, alcoholism, urinary losses
  • effects = behavioral changes, irritability, increased reflexes, muscle cramps, unsteady gait, nystagmus, tetany, convulsions, tachycardia, hypotension
82
Q

Hypermagnesemia

A
  • causes = usually renal insufficiency or failure, also excessive intake of magnesium - containing antacids, adrenal insufficiency
  • effects = spasms, excess nerve function, loss of deep tendon reflexes, nausea and vomiting, muscle weakness, hypotension, bradycardia, respiratory distress
83
Q

Calcitonin

A
  • function = lowers serum calcium levels, lowers serum phosphate levels, decreases calcium and phosphorus absorption in the GI tract
  • regulation = stimulated by elevated serum calcium levels, stimulated by gastrin, Ca+ rich foods, pregnancy, suppressed by low serum calcium levels
84
Q

Parathyroid hormone

A
  • function = regulate serum calcium concentration, overall effect is to increase serum calcium and decrease serum phosphate, acts directly on the bone to release calcium by stimulating osteoclast activity, acts on the kidneys to increase calcium reabsorption and decrease phosphate reabsorption
  • regulation = stimulated by a decrease in serum ionized calcium levels, increased serum calcium concentration inhibit PTH secretion
85
Q

Endocrine pancreas

A
  • both endocrine (release hormone into blood) and exocrine (secrete pancreatic juice)
  • the islets of Langerhans
    1) secretion of glucagon and insulin
    2) alpha cells = glucagon
    3) beta cells = insulin
    4) delta cells = somatostatin and gastrin
    5) F cells = pancreatic polypeptide
86
Q

Alpha cells

A
  • 20% of cells
  • secretes glucagon hormone
  • glucagon converts glycogen to glucose in the liver
  • raises the blood glucose level
87
Q

Beta cells

A
  • 70% of cells
  • secretes insulin
  • insulin lowers blood glucose levels
88
Q

Delta cells

A
  • 10% of cells
  • secretes somatostatin which inhibits glucagon and insulin secretions
  • secretes gastrin which metabolizes fats and CHO
89
Q

Insulin

A
  • a hormone is released in response to increased blood glucose levels
  • insulin secretion is controlled by a negative feedback system
  • negative feedback system is rapid acting and works within minutes
90
Q

how insulin works

A
  • facilitated diffusion (carrier transport)
  • insulin transports glucose across cell membrane
  • at target cell, insulin combines with receptor on surface of membrane
  • this activates glucose transportation within seconds into the cell
91
Q

effects of insulin on the liver

A
  • insulin facilitates the uptake of glucose
  • this leads to the formation of glycogen (inactive glucose) and fat stores in the liver
  • when blood glucose decreases, liver cells release glucose by process of glycogenolysis (breaks down glycogen to glucose)
92
Q

effects of insulin on adipose tissue

A
  • promotes fat storage by increasing transport of glucose into fat cells and increasing fat storage in adipose tissue
  • insulin stops release of fatty acids into circulation by increasing fat transport into cells
93
Q

effects of insulin on muscle

A
  • insulin increases the transport of glucose across membrane into muscle cell
94
Q

corticosteroids

A
  • can give someone diabetes with these
  • increases blood sugar by increasing the production of glucose from the liver and production of glucagon (stores glucose)
95
Q

glucocorticoids

A
  • stimulates glucose formation
  • cause protein catabolism and liver gluconeogenesis (formation of glucose in the liver)
96
Q

Catecholamines

A
  • fight or flight
  • increase in gluconeogenesis (production of active glucose)
  • causes hyperglycemia
  • decreases glucose use by muscle fats
  • decrease insulin release from beta cells
  • need fast energy
97
Q

role of glucagon

A
  • stimulates the conversion of glycogen to glucose in the liver
  • opposite effect of insulin
  • so low blood glucose will stimulate secretion of glucagon
98
Q

Type 1 (IDDM)

A
  • juvenile diabetes
  • absolute insulin deficiency
  • destruction of all beta cells in the pancreas
99
Q

Type 2

A
  • adult onset
  • may develop as a result of lowered sensitivity to insulin
  • receptors don’t recognize insulin
  • decrease insulin production r/t age
  • risk increases with age, obesity, bad diet
100
Q

secondary diabetes

A
  • associated with other conditions
  • chronic pancreatitis or pancreatic CA
  • drug induced: chronic steroid therapy
101
Q

gestational diabetes

A
  • first recognized during pregnancy
  • glucose may normalize after delivery
  • 60% of women with gestational diabetes with develop diabetes within 15 years
  • due to metabolic demands of the fetus
102
Q

Glycosylated hemoglobin

A
  • test that measures the amount of HbA1c (hemoglobin into which glucose has been incorporated) into the blood
  • HbA1c measures the levels of blood glucose levels over the previous 2-3 months
103
Q

type one pathophysiology

A
  • characterized by autoimmune destruction of pancreatic beta cells
  • autoantibodies damage cells
  • absolute lack of insulin, elevation in blood glucose and breakdown of body fats and proteins
104
Q

type one causes

A
  • results from an interactions between genetic and environmental factors
  • environmental + genetic = cell mediated autoimmune destruction of beta cells
  • infection = viral, bacterial
  • body destroys own beta cells
105
Q

clinical manifestations of type one

A
  • polyuria = excessive urine output
  • polydipsia = excessive thirst
  • polyphagia = excessive hunger
  • weight loss d/t increased urination
  • fatigue and lethargy d/t poor use of carbohydrates
  • ketoacidosis = body shifts from carbohydrates metabolism to fat and protein, byproduct of fat breakdown is ketones, accumulation of ketones lead to metabolic acidosis
106
Q

type two pathophysiology

A
  • type two diabetics are overweight (80%) and older
  • obese clients have increased resistance to the action of insulin
  • increased body weight, increased insulin resistance
  • abnormal pancreatic islet cell functions – doesn’t recognize insulin
107
Q

type two causes

A
  • obesity
  • environmental factors
  • genetic - inherited deficiency of beta cells
  • decreased beta cell mass
  • surgery
108
Q

type two clinical manifestation

A
  • overweight
  • polyuria
  • polydipsia
  • polyphagia
  • recurrent blurred vision
  • fatigue
  • paresthesias
  • skin infections
109
Q

complications of chronic diabetes

A
  • neuropathic = loss of myelin, nerve degeneration and delayed conduction, sensory issues
  • microvascular = thickening of capillary basement membrane
  • retinopathy = the leading cause of blindness
  • nephropathy = the leading causes of end stage renal disease
  • higher risk of infection = lack of sensation, ischemia, decreased immune response, bacteria loves glucose, decreased perfusion, wounds heal slower
  • macrovascular = increased development of atherosclerosis r/t lack of insulin
110
Q

acute complication = hypoglycemia

A
  • blood glucose less than 50mg/dL
  • d/t over administration of insulin or extreme exercise
  • decrease of significant glucose for neuronal use
  • hypothalamus stimulates SNS catacholamine release from adrenals
  • symptoms = neuro changes, pale, diaphoretic, tachycardia, seizure, coma, stroke-like symptoms
111
Q

acute complication = ketoacidosis

A
  • lack of insulin leads to mobilization of fatty acids from adipose tissue
  • this leads to ketone production by the liver which exceeds cellular use and renal excretion
  • incomplete breakdown leads to metabolic acidosis
112
Q

acute complication = hyperosmolar hyperglycemia nonketotic coma

A
  • characterized by hyperglycemia (blood sugar of greater than 600)
  • hyperosmolarity
  • severe dehydration
  • neurological complications
  • seizures
  • treated by IV fluids, then insulin
113
Q

pain systems

A
  • sensory/discriminative system – strength, intensity, temporal, and spatial aspects, removal of painful stimuli
  • motivational/affective system – individuals approach or avoidance to pain
  • cognitive/evaluative system – pain experience, how pain behavior is learned
114
Q

neuroanatomy of pain

A
  • afferent pathways = from PNS, travel to spinal cord and then ascend to higher centers in the CNS
  • interpretive centers = in brainstem, midbrain, diencephalon and cerebral cortex
  • efferent pathways = descend from CNS to outside (understanding sensation)
115
Q

Nociception

A
  • pain sensation
  • free nerve endings
  • respond to chemical, mechanical, and thermal stimuli
  • found under epidermis, within joint and bone surfaces, deep tissues, muscles, tendons
  • not evenly distributed
  • delta A fibers = sharp pain
  • C polymodal fibers = dull, achy pain
116
Q

endorphins

A
  • inhibit transmission of pain
  • block pain
  • similar feeling to opiates
  • can be achieved by: stress, physical activity, acupuncture, sexual activity, serotonin, raising pain threshold
117
Q

clinical descriptions of pain

A
  • somatogenic pain = pain with a cause; tissue injury, broken bones
  • psychogenic pain = pain with no physical cause, does not match symptoms; headache
  • etiologic pain = cause of pain
118
Q

acute pain

A
  • alerts an individual to a condition that is immediately harmful to the body
  • arises suddenly, relieved after underlying cause is corrected
  • acute anxiety is always associated with acute pain
  • causes individual to take prompt action to relieve pain
119
Q

classification of acute pain

A
  • acute somatic (delta A fibers) – arises skin, joint, muscles, carried by sensory nerve fibers, pain is well localized
  • acute visceral (C fibers) – pain in the internal organs in the abdomen or skeleton, poorly localized, often referred pain
  • referred pain – present in an area removed or distant from its point of origin, can be acute or chronic
120
Q

chronic pain

A
  • persistent or intermittent
  • may be sudden or develop insidiously
  • usually defined as lasting at least 3-6 months
  • response patterns vary greatly
  • learn to cope
  • body is overstimulated from pain, causing nonpainful stimuli to be painful
121
Q

common types of chronic pain

A
  • persistent low back pain
  • myofascial pain syndrome – spasms, tenderness and stiffness
  • chronic postoperative pain
  • cancer pain
  • phantom limb pain
122
Q

pain threshold and tolerance

A
  • pain threshold = point at which stimulus is perceived as pain
  • perceptual dominance = with multiple injuries, body can only focus on one at a time
  • pain tolerance – how long until pain is enough
123
Q

temperature regulation

A
  • achieved through balancing of heat production, conservation, and loss
  • varies in response to: location, activity, environment, circadian rhythm, gender
  • regulated by hypothalamus and thermoreceptors
124
Q

hypothalamic heat production

A
  • hypothalamus triggered by low temperature
  • stimulates anterior pituitary to release thyroid stimulating hormone causing release of thyroxine
  • thyroxine acts of adrenal medulla causing release of epinephrine
  • epinephrine causes vasoconstriction, stimulates glycolysis and increases metabolic rate, increasing heat production
125
Q

hypothalamic heath conservation

A
  • hypothalamus triggered by low temperature
  • stimulates the sympathetic nervous system
  • stimulates the adrenal cortex
  • increasing skeletal muscle tone and initiating shivering response and producing vasoconstriction
  • results in heat conservation
126
Q

Fever

A
  • temporary resetting of the hypothalamic thermostat to a higher level in response to stimuli
  • benefits of fever = kills of bacteria, decreases serum levels or iron, zinc, and copper, enhanced phagocytosis, releases antivirals, autodestruction of cells
127
Q

hyperthermia

A
  • elevation of the body temperature without an increase in the hypothalamus set point
  • can product nerve damage, coagulation of cell proteins, and death
  • heat cramps, heat exhaustion, heatstroke
128
Q

heat cramps

A
  • severe spasmodic cramps in the abdomen and extremities
  • follow prolonged sweating and associated sodium loss
  • common in individuals not accustomed to the heat or those performing strenuous work in warm climates
  • fever, rapid pulse, and increased blood pressure
129
Q

heat exhaustion

A
  • collapse as a result of prolonged high core or environmental temperatures
  • hypotensive, dehydrated, depressed plasma volumes
  • dizziness, weakness, nausea, confusion, syncope
130
Q

heatstroke

A
  • lethal result of an overstressed thermoregulatory center
  • cerebral edema, degeneration of the CNS, renal tubular necrosis, death, no sweating
131
Q

hypothermia

A
  • therapeutic hypothermia = used to slow metabolism and preserve ischemic tissue during surgery or limb re-implantation
  • accidental hypothermia = common result of sudden immersion in cold water or prolonged exposure to cold
  • vasoconstriction alternations in the microcirculation, coagulation, and ischemic tissue damage
  • ice crystals
  • tissue hypothermia – thickens blood
132
Q

sleep

A
  • temporary state of restful unconsciousness with spontaneous arousal
  • hypothalamus is the major sleep center
133
Q

REM sleep

A
  • 20-25% of sleep time
  • initiated by neurons in the pons
  • EEG brainwaves mimic the awake brain
  • increases PNS and varying SNS activity
134
Q

NREM Sleep

A
  • 75-80% of sleep time
  • sympathetic tone decreased
  • parasympathetic activity is increased resulting in = basal temperature decreases, HR,RR,BP and muscle tone decreases, pupils constrict, growth hormones released, corticosteroid and catecholamines levels are suppressed, decreased cerebral blood flow
135
Q

Dyssomnias

A
  • insomnia = inability to fall asleep or stay asleep
  • sleep disordered breathing = obstructive sleep apnea syndrome, upper airway obstruction recurring during sleep with snoring and apneic periods
  • hypersomnia = narcolepsy and r/t sleep disordered breathing or depression
  • circadian rhythm disorders = altered sleep–wake cycle

Pathophysiology Exams (2 decks)

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