Unit 1 Pathophysiology

Front 1

Pathophysiology definition

Back 1

Study of functional or physiologic changes in the body, that result from disease processes

Front 2

What factors can influence health?

Back 2

Age, gender, genetics, environment, and activity level

Front 3

Homeostasis mechanisms in the body

Back 3

Blood pressure, blood sugar, fluid balance, body temperature

Front 4

Can normal cellular adaptations be reversed

Back 4

Yes, but usually only after the stimulus is removed (hormones or environment)

Front 5

Why do abnormal cellular adaptations lead to disease

Back 5

Cell structure and function cannot be maintained which leads to changes in homeostasis. Can lead to irreversible cell changes which can become abnormal or malignant

Front 6

Atrophy

Back 6

Decrease in size of cell results in reduced tissue mass

Front 7

Hypertrophy

Back 7

Increase in the size of individual cells, resulting in enlarged tissue (CHF)

Front 8

Hyperplasia

Back 8

Increased number of cells resulting in increased tissue mass (increased cancer risk)

Front 9

Metaplasia

Back 9

One mature cell type is replaced by different mature cell type that is more resistant or stronger

Front 10

Dysplasia

Back 10

Tissue where cells vary in size and shape have large nuclei, and the rate of mitosis is increased (chronic irritation or pre-cancerous changes)

Front 11

Anaplasia

Back 11

Undifferentiated cells that don’t grow up

Front 12

Neoplasia

Back 12

New growth or tumor can be benign or malignant

Front 13

What causes cellular injury?

Back 13

Physical damage: excessive heat/cold or radiation exposure

Mechanical damage: pressure/tearing of tissue

Chemical toxins: exogenous (environment) or endogenous (inside the body)

Micro organisms, bacteria, or viruses

Abnormal metabolites or altered metabolism

Genetic disorders or inborn errors of metabolism

Nutritional deficits or imbalance of fluid and electrolytes

Front 14

Difference between hypoxia and ischemia

Back 14

Hypoxia is decreased oxygen in tissues and is the most common cellular injury while ischemia is decreased oxygenated blood flow to a tissue or organ (either locally like a blocked artery or systemically like anemia or pneumonia)

Front 15

Does cellular death cause inflammation

Back 15

Yes, and no. Apoptosis is programmed and contained so there is no inflammation. Necrosis causes injury to the cells around it leading to inflammation

Front 16

Process of apoptosis

Back 16

The cell shrinks and forms blebs that break off and macrophages perform phagocytosis

Front 17

Process of necrosis

Back 17

Damage to the cell is irreversible and the cell dies. The nucleolus disintegrates, the cell lysis, and releases lysosomal enzymes, which cause inflammation. Enzymes damage surrounding cells and can diffuse into the bloodstream

Front 18

Cellular injury process

Back 18

Decreased oxygen causes cellular swelling. If the stressor is taken away early, the cell reverts to normal, but if the stresser is greater damage or stays longer, that can lead to cellular death

Front 19

Purpose of the sodium potassium pump

Back 19

There is more potassium inside a cell and more sodium outside this out to begin. It uses ATP to move sodium in and potassium out during action potential then reverses

Front 20

What happens when the sodium potassium pump is broken?

Back 20

Sodium, calcium, and water all move into the cell and the cell swells with water until it ruptures (if oxygen level is restored or the problem is fixed, it can go back to normal)

Front 21

What causes lactic acid build up and what pH change happens

Back 21

Anaerobic metabolism increases lactic acid, which decreases the pH (acidosis)

Front 22

Difference between somatic and visceral pain

Back 22

Somatic pain originates in the skin, bone, or muscle and it is conducted by sensory nerves. Visceral pain originates in organs and is conducted by sympathetic fibers that transmit to the central nervous system

Front 23

What are nociceptors and how are they stimulated?

Back 23

Pain receptors for free sensory nerve endings for painful stimuli that are found in tissues throughout the body. They are stimulated by extreme temperatures, chemicals, or mechanical/physical stress

Front 24

Difference between afferent and efferent sensory nerve fibers

Back 24

Afferent fibers transmit pain to the spinal cord and brain (A-delta and C fibers)

Efferent fibers transmit from the central nervous system to muscles, glands, and organs (causes involuntary muscle contractions or reflex)

Front 25

Difference in A-delta and C fibers

Back 25

A delta fibers transmit acute pain quickly and are related to thermal or physical stimuli; usually from the skin or mucous membranes

C fibers are unmyelinated, so they transmit chronic pain slowly and can be related to thermal/physical/chemical stimuli from muscles/tendons/myocardium/digestive tract/skin

Front 26

Why is the efferent pathway faster than afferent?

Back 26

Efferent impulses travel from spinal cord synapse straight to muscles, causing an involuntary contraction (reflex) because of the danger the stimulus poses (touching hot stove). Afferent impulses go all the way to the brain and back down because there is no immediate danger (stubbing toe)

Front 27

What is the reticular formation and what makes it up?

Back 27

It creates awareness of pain

Hypothalamus - response to pain

Thalamus - process sensory stimuli

Parietal lobe - locate and characterize pain

Front 28

Explain the gate control theory

Back 28

There are gates built into pain pathways that are located at nerve synapses in the brain and spinal cord. They determine entry of pain stimuli into the spinal cord and brain. if gates are open, they permit pain impulses from the peripheral nerves to ascend to the brain and if gates are closed, it stops or reduces the passage of the pain impulse. only one type of impulse can go through the gate at a time. gate closure can occur in response to other sensory sensations like TENS, application of ice, massage, efferent transmissions

Front 29

How do endorphins block pain

Back 29

Attach to opiate receptors (they are natural opioids) on afferent neurons, which blocks the release of substance p (increases pain response) at the synapse and closes the gate

Front 30

Difference between the locations of pain

Back 30

Localized - source of pain can be identified as being in a specific area

Generalized - source of pain is difficult to determine

Referred - pain in area some distance from the source of the pain. Usually pain from a deep organ or a muscle that is felt on the surface of the body in a different area

Phantom - occurs after amputation, felt in the lost limb

Front 31

Pain is subjective, what may influence it

Back 31

Age, culture, prior experience, attitude of the day, persons temperament and personality, body image, family relationships

Front 32

Difference between acute and chronic pain

Back 32

Acute pain is sudden, severe and short and it indicates tissue damage. It is a stress response and has a strong emotional response. Chronic pain is long-term pain that leads to negative affects. It is harder to treat, more generalized, harder to manage, affects ADLs

Front 33

Cause of migraines

Back 33

Blood flow and metabolism changes in the brain

Front 34

What are intracranial headaches and what are the causes?

Back 34

Increased pressure inside the skull caused by edema, hemorrhage, tumors, infections, toxins that cause swelling

Front 35

Difference in the classifications of pain

Back 35

Central pain - caused by an injury to the brain or spinal cord

Neuropathic - trauma or disease involving peripheral nerves

Ischemic - sudden loss of blood supply to an organ or tissue, leading to hypoxia and then tissue damage. Inflammation leads to pain releasing substances.

Cancer related - advanced cancer is putting pressure on tissues, causing inflammation to obstruct vessels, ducts, and intestines

Front 36

Why is water balance essential?

Back 36

It helps maintain homeostasis, metabolic reactions, cushions joints and aids and movements of the lungs, transportation (Carries nutrients to cell, wastes away from cell, and blood cells around the body)

Front 37

If a patient has congestive heart failure or kidney disease, what happens to the volume of fluid

Back 37

They are at risk for fluid overload, which would put them into respiratory distress

Front 38

Which hormones and organs, maintain fluid balance

Back 38

Hypothalamus - thirst mechanism

Antidiuretic hormone - controls fluid, leaving the body in urine and promotes reabsorption into kidney tubules

Aldosterone - when sodium or blood pressure is low, it promotes the reabsorption of water and sodium in kidney tubules

Natriuretic peptide hormones (ANP and BNP) - released by cardiac muscles during fluid overload to stimulate urination of sodium and water

Front 39

How does the hypothalamus and ADH conserve fluid

Back 39

Osmoreceptors in the hypothalamus sense low body fluid in the hypothalamus produce is ADH. The pituitary gland releases it and that circulates to the kidneys. Kidney since the ADH and reabsorb water into the bloodstream

Front 40

How does aldosterone conserve fluid and when is it released?

Back 40

It is released when potassium is high and sodium is low. It reabsorbs sodium and water in kidney tubules and excretes potassium

Front 41

When are natriuretic peptides released

Back 41

Released due to increased blood volume. It stimulates the release of sodium and water, decreases the workload on the heart (decrease BP), and inhibits the release of ADH and aldosterone.

Front 42

Explain capillary hydrostatic and osmotic pressure

Back 42

Hydrostatic pressure is higher at the arterial end of the capillary and pushes fluid out. Osmotic pressure is higher at the venous end and pulls fluid into the capillary

Front 43

What are the two types of edema? (in relation to the type of fluid)

Back 43

Transudative - low protein, watery fluid

Exudative - high protein count (albumin)

Front 44

What is the role of albumin?

Back 44

Albumin pulls water back into the capillary so if they get out of the capillary, water cannot get back in

Front 45

Explain the four causes of edema

Back 45

Increased capillary hydrostatic pressure - fluid volume increase so hydrostatic pressure remains high at the venous end of the capillary an osmotic pressure cannot pull fluid back in. Leads to transudative putting edema.

Decreased capillary osmotic pressure - decreased albumin production, so fluid stays and interstitial area. Leads to transudative nonpitting edema.

Increased capillary permeability - capillary endothelial cell injury leads to inflammatory response and the release of histamine. Endothelial gap forms and increases capillary permeability allowing fluid and albumin to leak. Leads to exudative edema.

Obstruction of the lymphatic system - extra fluid in the interstitial area is unable to drain into the lymphatic system leading to localized edema

Front 46

What are the signs and symptoms of edema?

Back 46

Localized swelling, pale or red skin, weight gain, slower bounding pulse, increased blood pressure, lethargy or seizures if the brain is involved, pulmonary congestion/cough/rales, high-volume and low specific gravity of urine, decreased lab values due to dilution (hematocrit, hemoglobin, and sodium levels)

Front 47

Effects of edema

Back 47

Functional and arterial circulation and impairment, pain, skin breakdown

Front 48

State the levels of sodium that to find which type of dehydration exists (iso, hypo, hyper)

Back 48

Isotonic dehydration - Na 135 to 145

Hypotonic dehydration - Na less than 135

Hypertonic dehydration - Na greater than 145

Front 49

Dehydration signs and symptoms

Back 49

Dry mucous membranes in the mouth, decreased skin turgor, decreased blood pressure, weak pulse, fatigue, increased hematocrit and hemoglobin, decreased mental functions

Front 50

Explain third spacing

Back 50

Fluid shifts out of the blood into the body cavity or tissue, causing a fluid deficit in the blood, but an increase in the interstitial area

Front 51

What is sodiums normal value and where is it normally found

Back 51

135 to 145 mEq/L and is primarily found in the extra cellular fluid compartment

Front 52

What does sodium do in the body?

Back 52

Conducts nerve impulses and muscle contraction and is the most prevalent cation an extracellular fluid so it maintains the extracellular fluid volume

Front 53

What hormone controls sodium and potassium levels

Back 53

Aldosterone

Front 54

Hyponatremia cause and effects

Back 54

The cause is a loss of sodium in the blood or excessive water gain. Effects (SALTLOSS) stupor, anorexia, lethargy, tendon and reflex weakness, limp muscles, orthostatic hypotension/hypovalemia, seizures/headaches, stomach/muscle contraction

Front 55

What is the main concern with high or low potassium levels

Back 55

Potassium imbalances cause cardiac arrhythmias, which can be life-threatening

Front 56

What is the normal level of potassium and where is it primarily located?

Back 56

Normal value is 3.5 to 5 mEq/L and is located intracellularly

Front 57

Potassium functions in the body

Back 57

Nerve conduction, muscle contraction, maintains intracellular fluid volume

Front 58

What happens to pH and potassium as hydrogen increases

Back 58

The pH goes down, becoming more acidic and causing H ions to shift from the blood to the cells and K moves out of the cell (hyperkalemia)

Front 59

What happens to pH and potassium as hydrogen decreases

Back 59

PH goes up, becoming more alkaline and causing potassium to move from the blood into the cell (hypokalemia)

Front 60

Relationship between phosphate and calcium

Back 60

They have a reciprocal relationship, so when calcium is high phosphate is low and vice versa

Front 61

How is calcium homeostasis maintained?

Back 61

If levels are too high, calcitonin is released (decreases reabsorption and increases calcium deposits in the bone). If levels are too low, PTH is released (increases reabsorption and calcium is released from bones)

Front 62

How does hypoparathyroidism affect calcium

Back 62

Decreased PTH leading to hypocalcemia

Front 63

Positive Chevostek sign/trousseau signs indicate

Back 63

Hypocalcemia

Front 64

Effect of hypercalcemia on the heart

Back 64

Contraction strengthens and dysrhythmias can develop, increased blood pressure

Front 65

Affects of hypo and hypermagnesemia

Back 65

Hypo - causes neuromuscular, hyperirritability, tremors, and insomnia

Hyper - causes depressed neuromuscular function and reflexes and lethargy

Front 66

Normal pH range, CO2 range, HCO3 range

Back 66

pH - 7.35 to 7.45

Co2 - 35 to 45

Hco3 - 22 to 26

Front 67

Relationship between the number of hydrogen ions and pH

Back 67

PH is inversely proportional to the number of hydrogen ions. If hydrogen ions go up, pH goes down (more acidic) and if hydrogen ions go down, pH goes up (more alkalotic)

Front 68

Three mechanisms that control pH

Back 68

The buffer system (fastest)

Respiratory system

Kidneys (slowest, but most efficient)

Front 69

What happens to CO2 and HCO3 in the four acid base imbalances

Back 69

Respiratory acidosis - pH low, Co2 high, Hco3 normal

Respiratory alkalosis - pH high, Co2 low, Hco3 normal

Metabolic acidosis - pH low, Co2 normal, Hco3 low

Metabolic alkalosis - pH high, Co2 normal, Hco3 high

Front 70

Respiratory acidosis cause, effect, compensation, laboratory values

Back 70

Cause - slow shallow respirations, respiratory congestion

Effect - increase in Co2 (above 45)

Compensation - kidneys excrete hydrogen and reabsorb bicarbonate

Laboratory - elevated Co2

Front 71

Respiratory alkalosis cause, effect, compensation, lab values

Back 71

Cause - hyperventilation

Effect - Co2 below 35

Compensation - kidneys excrete less hydrogen and reabsorb less bicarbonate

Lab values - low Co2

Front 72

Metabolic acidosis cause, effect, compensation, lab values

Back 72

Cause - shock, diabetic ketoacidosis, renal failure, diarrhea

Effect - decreased serum bicarbonate (below 22)

Compensation - rapid deep respirations, kidneys excrete more acid and increase bicarbonate reabsorption

Lab values - low serum bicarbonate

Front 73

Metabolic alkalosis cause, effect, compensation, lab values

Back 73

Cause - vomiting, excessive antacid intake

Effect - increased serum bicarbonate (above 26)

Compensation - slow shallow respirations, kidneys excrete less acid and decrease bicarbonate absorption

Lab values - elevated serum bicarbonate