Medical Flashcards

1
Q

what are the tetracannaboids (nabilone used for at the end of life)

A

category: antiemetic

used for N & V associated with chemotherapy

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2
Q

what are the anticholinergics and what are they used for

A
  • scoplamine
  • hyoscine butylbromide
  • glycopyrrolate
  • used for management of excess oral secretions when death is imminent
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3
Q

examples of neuroleptics (antipsychotics) and what they are used for?

A
  • Chlorpromazine
  • Methotrimeprazine
  • Haloperidol
  • for treating delirium at the end of life
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4
Q

Benzodiazpeines for end of life

A

Midazolam: off label use is palliative sedation

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5
Q

Opiods for end of life

A
  • Morphine (low doses of opiods are very effective in decreasing preception of dyspnea, presumably by decreasing sensory preception as they do with pain) & pain
  • Fentanyl: Pain
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6
Q

Key points of DKA:

A
  • no insulin therefore gluconeogensis & lipolysis

- production of ketone bodies (acetone breath) & ketoacidosis (can be severe)

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7
Q

Key points of HHS:

A
  • insulin still present therefore gluconeogensis & lipolysis mainly inhibited
  • ketones mild/absent & normal pH
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8
Q

Signs of approaching death?

A
  • person will show less interest in eating or drinking
  • urinary output may decrease in amount & frequency
  • as body weakens patient will sleep more & begin to deattach from environment
  • mental confusion will become apparent , as less oxygen available to supply brain
  • vision & hearing become somewhat impaired & speech may be difficult to understand
  • secretions may collect in the back of the throat & rattle & gurgle as the patient breathes through mouth
  • breathing may become irregular with periods of no breathing (apnea)
  • as oxygen supply to the brain decreases the patient may even become restless
  • the patient may feel hot one moment & cold the next as he or she loses the ability to control body temp
  • loss of bladder & bowel control may occur at time of death
  • as people approach death, many times they report seeing, gardens, libraries or friends who have died
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9
Q

physiologic changes near the end of life?

A
  • weakness/fatigue
  • decreasing appetite/food intake, wasting
  • decreased fluid intake, dehydration
  • decreased blood perfusion, renal failure
  • neurologic dysfunction, decreasing LOC, terminal delirium, changes in resp, loss of ability to swalloe
  • loss of sphincter control
  • loss of ability to close eyes
  • changes in medication needs
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10
Q

Results of HHS & DKA

A

-hyperglycemic state
-osmotic diuresis mainly due to glucose
DKA: ketones & acidosis
HHS: no ketones & normal pH (but typically greater fluid loss)

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11
Q

Signs & symptoms of DKA

A
  • acetone breath
  • ketones in urine
  • acidosis
  • confusion/coma all from ketone production
  • kussmaul breathing (deep rapid breathing)
  • abd pain form metabolic acidosis
  • polyuria from high glucose (osmotic diuresis)
  • glucose in urine, polydipsia & tachycardia from dehydration
  • sodium may be increased/decreased or norm
  • hypotension from dehydration
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12
Q

Signs & symptoms of HHS

A
  • negative ketone breath & no ketones in urine becuase no lipolysis (no breakdown of fat) therefore no ketone production
  • stupor/coma from hyperosmolare state
  • fluid imbalance (dehydration/sodium, polyuria form high glucose (osmotic diuresis)
  • glucose in urine
  • polydipsia & tachycardia form dehydration, Hypotension, profound dehydration, dry mucous membranes
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13
Q

what is happening with DKA & HHS

A
  • glucagon secretion not inhibited
  • elevated glucose levels continue to rise
  • state of absolute or relative lack of insulin
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14
Q

brief on DKA

A
  • type 1 & 2 (most common in type 1)
  • can develop quickly in less than 24 hours
  • BG: greater than 13.9mmol/L
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15
Q

how do you treat DKA

A

HIE
hydration
insulin
electrolyte replacement

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16
Q

Brief on HHS

A
  • mostly in type 2 (sometimes in one), also in older people with no history of diabetes or mild T2DM
  • develops more slowly than DKA (days -weeks)
  • blood glucose (greater than 33.3 mmol/L)
17
Q

HHS has a higher

A

mortality rate than DKA

18
Q

HHS treatment

A

similar to DKA
hydration
insulin
electrolyte replacment

19
Q

preventing complications with treatment OF HHS & DKA

A

-dropping glucose too fast can cause cerebral edema, fluid shifts into the brain, may become apparent with decreased LOC

20
Q

what are the causes of DKA & HHS?

A

Usually a stressful event that causes the release of glucagon, cortisol & catecholmines:

  • infection
  • MI
  • Treatment errors with insulin
  • Diarrhea & vomiting
  • Stroke
  • tramua
  • pancreatitis
  • uknown etiology
  • continue to check BS & give yourself insulin when sick