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Pathophysiology > Module 1 part 2 > Flashcards

Module 1 part 2 Flashcards

1
Q

Nociceptors

A

Are free nerve endings that respond to stimuli: Chemical, mechanical, thermal

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2
Q

Pain transduction begins when tissue is damaged by exposure to chemical, mechanical, or thermal noxious stimuli. This causes activation of nociceptors, which are free nerve endings in the afferent peripheral nervous system that selectively respond to different types of stimuli. Where are they located?

A 
Throughout the body but are not evenly distributed so the relative sensitivity to pain differs according to their location. Under epidermis
Within joint & bone surfaces
Deep tissues
Muscles
Tendons
Subcutaneous tissue
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3
Q

Activation of nociceptors causes what?

A 
Ion channels (sodium, calcium) to open, creating electrical impulses that travel through two primary types of nociceptors: A-delta fibers and C fibers. The medium sized thinly myelinated A-delta fibers rapidly transmit sharp, well-localized "fast" pain sensations. These are responsible for causing reflex withdrawal of the affected body part from the stimulus before a pain sensation is perceived. The smaller unmyelinated C fibers slowly transmit dull, aching, or buring sensations that are poorly localized & often constant.
-A-beta fibers are large myelinated fibers that transmit touch & vibration sensations. Normally don't transmit pain , but play a role in modulation
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4
Q

Nociceptors can be sensitive to?

A
  • extremes of temperature
  • mechanical damage
  • dissolved chemicals, such as chemicals released by injured cells
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5
Q

Specificity Theory Of Pain

A

The intensity of pain is directly related to the amount of associated tissue injury.
More relevant with specific injury and acute pain
Less reliable for chronic pain or cognitive contributions to pain

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6
Q

Neuromodulators

A
  • Substances that influence pain
  • Can be triggered by
    • Tissue injury
    • Chronic inflammatory lesions
      1) Excitatory Neuromodulators
    • Substance P
      2) Inhibitory Neuromodulators
    • GABA
    • Norepinephrine
    • Endorphins
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7
Q

Excitatory neuromodulators

A

Excitatory neuromodulators include such substances as substance P, histamine, glutamate, and calcitonin gene-related peptide.
-these substances sensitize nociceptors in the PNS or CNS leading to an increased responsiveness & reduced threshold of nociceptors that cause them to fire w/increased frequency, resulting in hyperalgesia (increased sensitivity to painful stimuli) and allodynia, the perception of innocuous stimuli. A progressive buildup of repeated stimulation of neurons in the dorsal horn by peripheral nerves leads to wind-up, which can result in pathologic changes in the CNS, prolonged pain, & increased sensitivity to future pain in the same location

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8
Q

Inhibitory neuromodulators

A

Include gamma-aminobutyric acid (GABA), glycine, 5-hydroxytryptamine (serotonin), norepinephrine, and endogenous opoids

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9
Q

Endogenous opioids: endorphin

A

endogenous opioids are a family of morphine-like neuropeptides that block transmission of pain impulses in the spinal cord, brain, and periphery by binding w/specific opioid receptors, kappa, and delta. They inhibit the release of excitatory neurotransmitters, such as substance P in the dorsal horn or in other areas of the brain, and may also be responsible for general sensations of well-being.
Endorphin is B-endorphin, purported to produce the greatest sense of exhilaration as well as substantial natural pain relief. It is a strong U receptor agonist.

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10
Q

Endorphins (main points)

A
  • Inhibitory Neuromodulator
  • Attach to opiate receptors
    • In afferent neurons
    • Inhibits release of excitatory neurotransmitters
    • Raises pain threshold
    • Opiate drugs
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11
Q

Types of acute pain

A

1) Somatic: Arising from skin.
- Superficial - Musculoskeletal
- Sharp(er) & well localized
- Sensory nerves
2) Visceral
- Internal organs or blood vessels
- Dull(er) & more poorly localized
- Sympathetic nerve fibers
3) Referred
- Pain distant from point of origin

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12
Q

Acute pain is a?

A

Protective mechanism that alerts the individual to a condition or experience that is immediately harmful to the body and mobilizes the individual to take prompt action to relieve it. It is transient, usually lasting seconds to days, sometimes up to 3 months
-Begins suddenly & is relieved after chemical mediators that stimulate pain receptors are removed

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13
Q 
Electrolytes 
Major component in fluid balance
Hydrostatic Pressure - pushes water _?_
Osmotic Pressure - draws water _?_
Oncotic pressure = 
Which organ produces proteins in blood that helps to hold water in?
A

Major component in fluid balance
Hydrostatic Pressure - pushes water out of the capillaries
Osmotic Pressure - draws water into the capillaires
Oncotic pressure = osmotic pressure exerted by proteins in a blood vessel’s plasma (blood/liquid) that usually tends to pull water into the circulatory system.
- Which organ produces proteins in blood that helps to hold water in? Liver

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14
Q

Electrolytes
Predominant intracellular:
Predominant extracellular electrolyte:

A

Predominant intracellular: K

Predominant extracellular electrolyte: Sodium

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15
Q 
Sodium main points
Then answer these questions:
1) Helps to?
2) Sodium important for?
3) Aldosterone tells kidney to?
4) ANP/BNP go to kidney and tells it?
A
  • 135-145 mEq/L
  • Major cation outside of the cell 90%
  • Maintains ECF osmotic balance
  • Function
    • Maintain tonicity of ECF
    • Facilitate nerve conduction and glandular secretions
  • Organs and Hormones involved
    • Kidney
    • Aldosterone
    • ANP/BNP
  • Most often goes hand in hand with chloride
    1) hold water
    2) action potential (depolarization)
    3) save sodum
    4) get rid of sodium
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16
Q

Sodium Functions
Then:
Fill in the blanks given the scenario below:
When a patient has hyponatremia, the extracellular osmolarity will 1) _______
When extracellular osmolality decreases water moves 2)________ the intracellular space - the most affected being brain– leading to cerebral 3)____________ (swelling)
The distribution of water and solute in the intracellular and extracellular spaces also determine the intravascular volume
If a patient is hyponatremic , there is 4)_______ in intravascular volume which may result in 5)___________tension.
You would then expect HR to 6)________. This is called 7)____________________

A
  • Involved in generating action membrane potential of cells
  • Makes a major contribution to extracellular osmolarity

1) Decrease
2) into
3) edema
4) decrease
5) Hypo
6) Increase
7) Tachycardia

17
Q

Hyponatremia

A 
Causes:
-Vomiting/Diarrhea
-Diuretics (most cause Na+ loss)
-Decrease Na+ in diet
-Prolonged sweating
-TBW increases more than Na+ i.e. exercising with H2O -- intake and no Na+ intake
-Kidney, Heart/liver dysfunction
Symptoms:
-Lethargy 
-Headaches
-Confusion
-Restlessness/Irritability 
-Muscle weakness, spasms
-Coma
18
Q

Hypernatremia >145 mEg/L
Causes:
Symptoms:
-too much sodium and aldosterone (sodium saver) might be cause of?

A 
Causes:
- ↑ Na: over-secretion of aldosterone, Cushing’s, increased dietary Na+
- Too little H2O
- Elderly/Infants
- Diabetes insipidus
- ↓ ADH
Symptoms:
- Thirst
- Restlessness
- Dry mucous membranes 
- Oliguria: Low output of urine
- Tachycardia
- Muscle twitching
- Hyperreflexia
- Convulsions 
-too much sodium and aldosterone (sodium saver) might be cause of tumor on anterior pituitary gland, because this releases ACTH
19
Q

Potassium

A
  • 3.5-5.0 mEq/L (ECF)
  • Major cation inside of cell (95-98%)
  • Function
    • Maintains ICF osmotic balance
    • Glycogen/glucose deposition: Liver and skeletal muscle
    • Transmission of nerve impulses
    • Maintenance of normal cardiac rhythms, skeletal and smooth muscle contractions
  • Organs and Hormones involved
    • Kidney
    • Aldosterone
  • K is important for normal resting membrane potential and action potentials
  • Important for heart rate, especially the pace maker of the heart
  • Kidney is major organ that gets rid of or hangs onto it
20
Q

What hormone drives sugar and K+ into a cell?

A

Insulin

21
Q

Potassium functins

A
  • The greatest contributor to intracellular osmosis and cell volume
  • Determines the resting membrane potential of a cell
  • Plays a role in blood pH by affecting the plasma concentration of H+
  • Determine what happens to the resting membrane potential if extracellular potassium rises?
  • Determine what happens to extracellular potassium levels if blood pH drops?
22
Q 
S/S:
Lethargy 
Headaches
Confusion
Restlessness/Irritability 
Muscle weakness, spasms
Coma
A

Hyponatremia

23
Q

Hyponatremia causes

A 
Causes
Vomiting/Diarrhea
Diuretics
Decrease Na+ in diet
Prolonged sweating
TBW increases more than Na+ i.e. exercising with H2O intake and no Na+ intake
Kidney, Heart/liver dysfunction
24
Q

S/S of hypernatremia

A 
S/S:
Thirst
Restlessness
Dry mucous membranes 
Oliguria
Low output of urine
Tachycardia
Muscle twitching
Hyperreflexia
Convulsions
25
Q

Causes of hypernatremia

A 
Causes
↑ Na: oversecretion of aldosterone, Cushing’s, increased dietary Na+
Too little H2O
Elderly/Infants
Diabetes insipidus
↓ ADH
26
Q

Causes of hypokalemia

A

Causes

  • ↑ Na: oversecretion of aldosterone, Cushing’s, increased dietary Na+
  • Too little H2O
  • Elderly/Infants
  • Diabetes insipidus
  • ↓ ADH
27
Q

S/S of hypokalemia

A

Signs and Symptoms
Muscle weakness and cramps
Arrhythmias – Shallow T wave

28
Q

Causes of hyperkalemia

A
  • Causes
    • Increased intake of K+
    • Ingestion of potassium salt
    • Salt alternatives
    • Increased exit of K+ from cells
    • Trauma – burns!
    • Acidosis
    • H+ enters cell and kicks out K+ into ECF to raise blood pH
    • Insulin deficiency *Insulin: K+ into ICF
    • Decreased renal excretion of K+
    • Renal failure
    • Addison’s disease
    • K+ sparing diuretics
    • Works by stimulating Na+ excretion and K+ reabsorption in the DCT – water follows Na+
29
Q

S/S of hyperkalemia

A

Signs and Symptoms
Weakness/Paralysis
Arrhythmias - Widened QRS & Tall peaked T wave

30
Q

Hyperkalemia Electrophysiological Explanation

A
  • Hyperkalemia  decreased K+ gradient between the inside and outside of the cell  inside of the cell more positive than normal (due to it retaining more K+)
  • Na+ channels are quickly opened as the membrane potential becomes more positive
  • Quickly after their fast-acting activation gate opens, the slow-acting inactivation gate closes and stays closed until repolarization occurs (the second gate is the reason for the refractory period after an AP).
  • So, in hyperkalemia, a greater number of Na+ channels are closed compared with a normal cell (due to the closing of the slow-acting gate)
  • Stronger stimulus needed to initiate an AP now that less Na+ channels are available to get the membrane potential to threshold

Pathophysiology (22 decks)

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