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IC 1.0 > Geriatrics > Flashcards

Geriatrics Flashcards

1
Q

What is aging?

A

the process that converts healthy adults into frail older persons with diminished reserves in most physiologic systems and increased vulnerability to most diseases

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2
Q

What are the four major features of aging?

A

it is:

  • destructive
  • progressive
  • partly determined by genetic code
  • and universal
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3
Q

What is usual aging?

A
  • a more step-wise form of aging that involves a gradual, consistent decline towards death
  • chronically ill or multimorbid as diseases add up until death
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4
Q

What is successful aging?

A

aging in which there is preserved function and compression of morbidity (long relatively slow decline that ends in a sharp drop off to death)

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5
Q

At what point in our lives are we all most alike? Least alike and most heterogenous?

A

at birth we are biologically very similar and our heterogeneity increases with age

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6
Q

What part of a history should follow the review of systems if you are dealing with a geriatric patient? Why?

A

a review of function because these patients have increasing frailty and vulnerability and an therefore an increased risk of impaired function

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7
Q

What is homeostenosis?

A

a term used to describe a reduced physiologic reserver and a resulting diminished ability to maintain homeostasis during periods of stress

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8
Q

What five vision changes are common during the aging process?

A
  • decreased dynamic visual acuity
  • decreased detection of lateral motion
  • decreased depth perception
  • decreased contrast sensitivity
  • increased glare sensitivity
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9
Q

How do vision changes impact the daily lives and medical care of geriatric patients?

A
  • reduces quality of life
  • eliminates the possibility of night driving
  • increases risk of falls
  • causes medication issues (finding pills, reading labels, etc.)
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10
Q

What is presbycusis? Describe it’s onset.

A
  • the loss of high frequency hearing that occurs with normal aging
  • it is slowly progressive, bilateral, and symmetrical
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11
Q

What is presbystasis?

A
  • the “dysequilibrium of aging”
  • characterized by vestibular degeneration
  • it is a diagnosis of exclusion
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12
Q

What two auditory changes are common during the aging process?

A
  • presbycusis (loss high frequency hearing)

- presbystasis (dysequilibrium of aging)

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13
Q

How do the changes in hearing that accompany aging affect geriatric quality of life?

A

it contributes to social isolation, loss of self-esteem, depression, anger, and family discord

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14
Q

How do taste and smell change with aging?

A

the threshold for tasting salty and sweet rise

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15
Q

How does the increased threshold for tasting salty and sweet impact the health of geriatric patients?

A
  • take less pleasure in eating and therefore eat less, contributing to weight loss
  • add more salt to their diet, potentially contributing to heart failure or hypertension
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16
Q

Name 6 geriatric changes that contribute to physiologic anorexia of aging?

A
  • reduced physical activity
  • diminished metabolism
  • reduced stretch of the gastric fundus, resulting in early astral filling
  • slowed gastric emptying
  • increased circulating CCK
  • decrease in dynorphins, which regulate eating drive
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17
Q

How does the esophagus change with aging?

A
  • poor swallowing coordination

- presbyesophagus (low amplitude contractions)

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18
Q

What contributes to reduced swallowing coordination in geriatric populations?

A
  • reduced facial strength
  • reduced lingual pressure reserve
  • pharyngeal swallow delay
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19
Q

What is presbyesophagus?

A

an age-related decreased in contractile amplitude within the esophagus

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20
Q

At what age might effective esophageal contractions be absent?

A

after age 80

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21
Q

Why are esophageal changes an important consideration in geriatric populations?

A

because they increase the risk of micro aspiration and can contribute to physiologic anorexia of aging

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22
Q

List four gastric changes that are seen over the course of normal aging?

A
  • decreased HCl
  • delayed gastric emptying
  • reduced intrinsic factor production
  • disruption of the gastric mucosal barrier
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23
Q

Why are geriatric patients more at risk for a B12 deficiency?

A

because they produce less intrinsic factor

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24
Q

What gastric conditions are geriatric patients more likely to have because of changes in their mucosal barrier?

A
  • atrophic gastritis

- peptic ulcer disease

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25
Q

Name 6 micronutrients that geriatric patients have reduced absorption of from the small bowel.

A
  • iron
  • zinc
  • B12
  • folic acid
  • lactose
  • vitamin D
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26
Q

What contributes to a vitamin D deficiency in aging patients?

A
  • reduced vitamin D receptors in the gut
  • less efficient production in the skin
  • less exposure to UV light
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27
Q

What changes are commonly seen in the colon/rectum of geriatric patients?

A
  • altered coordination of contractions
  • increased compliance
  • reduced rectal sensation
  • diverticulosis
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28
Q

What colonic changes make diverticulosis more common in geriatric patients?

A
  • decreased tensile strength of bowel wall
  • slowed transit through the bowel
  • poor coordination of contractions in the bowel
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29
Q

Why do geriatric patients have a lower defecation urge? What problems does this pose?

A
  • increased rectal compliance
  • decreased rectal sensation
  • may contribute to more frequent constipation
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30
Q

Why are geriatric patients at higher risk for constipation?

A
  • because they have increased rectal compliance and decreased rectal sensation
  • as a result a larger stool volume is needed for a defecation urge
  • stool frequency declines and stool hardness increases
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31
Q

How do LFTs change with age?

A

they do not; you still need to work them up if they change

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32
Q

How does bile change in geriatric patients?

A

they have a predisposition toward cholelithiasis because their bile has a higher lithogenic index

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33
Q

How does liver function change in geriatric populations?

A
  • drug clearance is reduced as the oxidative and P450 pathways are diminished
  • less synthesis of vitamin-K dependent clotting factors
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34
Q

Why are benzodiazepines avoided in geriatric patients?

A
  • because their metabolism and clearance is greatly inhibited by the slowed oxidative pathway in the liver, leaving these drugs in the system for a very long time
  • additionally there appears to be an increase in receptor sensitivity in geriatric populations
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35
Q

How does the pancreas change during normal aging?

A

pancreatic exocrine function, absorption of fats, and absorption of carbohydrates is unchanged

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36
Q

Which GI organ remains unchanged with normal aging?

A

the pancreas

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37
Q

How does the heart change with normal aging?

A
  • systemic vascular resistance increases
  • LV diastolic filing is decreased as a result of lower LV compliance and greater thickness
  • as such, there is a greater reliance on atrial kick for ventricular filling
  • maximal heart rate decreases
  • maximal cardiac output decreases
  • exercise vasodilation response decreases
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38
Q

How does systemic vascular resistance change with normal aging?

A

it increases as arterial compliance diminishes

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39
Q

The geriatric heart has a greater reliance on what diastolic action? Why?

A
  • atrial kick

- because the LV is thicker and less compliant, so passive filling is impaired

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40
Q

To what degree does LV filling decline with age?

A

50% between the ages of 20 and 80

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41
Q

Is systolic or diastolic cardiac functioning changed with geriatric age?

A

diastolic

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42
Q

Why does cardiac output decline in geriatric patients if systolic function is normally unchanged?

A

because filling is reduced and therefore so is stroke volume

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43
Q

Why are older adults more susceptible to atrial fibrillation?

A

because they are more reliant on atrial kick for ventricular filling and atrial fibrillation removes this contribution

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44
Q

Why do geriatric individuals take longer to recover from tachycardia/exertion?

A

because they have significantly reduced inotropic and chronotropic responses, prolonging recovery afterwards

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45
Q

How do geriatric patients compensate for a diminished chronotropic response to exertion?

A

they rely more on increases in stroke volume to compensate for reduced maximal heart rate

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46
Q

Do geriatric patients have a greater reserve for stroke volume or heart rate?

A

stroke volume

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47
Q

Why do geriatric patients have reduced arterial compliance?

A

because they have a thickened arterial intima due to calcium deposits, altered collagen and elastin, and smooth muscle hypertrophy

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48
Q

Which layer of geriatric arteries is thickened?

A

the intima

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49
Q

What kind of hypertension is most common amongst geriatric patients? Why is that?

A
  • isolated systolic hypertension

- because it is a result of reduced arterial compliance

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50
Q

Poorly controlled ISH is a risk factor for what three conditions?

A
  • CVA
  • MI
  • heart failure
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51
Q

Why are geriatric patients more at risk for orthostatic hypotension?

A
  • because they have diminished baroreceptor sensitivity
  • they also often have low blood volumes due to low thirst mechanisms or diuretics
  • they often have wider pulse pressures as well because of arterial compliance and ISH
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52
Q

By what age do the lungs fully expand only while standing?

A

by age 65

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53
Q

What age-related changes are seen in pulmonary function?

A
  • reduced chest wall compliance due to cartilage calcification
  • reduced muscle strength and cough effort
  • reduced mucocilliary clearance
  • reduced micro oropharyngeal aspiration
  • reduced alveolar surface area and elastic recoil
  • poor lung expansion with a dependence on abdominal breathing
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54
Q

Pulmonary changes associated with normal aging increase the risk for what three things?

A
  • atelectasis
  • reduced clearance of viruses and bacteria
  • pneumonia (aspiration or not)
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55
Q

What lung volume is expanded in geriatric patients? Why?

A

residual volume because compliance is increased and elastic recoil is decreased

56
Q

What lung volumes decrease with aging?

A
  • vital capacity
  • peak expiratory flow rate
  • FEV1
57
Q

Which part of the lungs are better perfused and ventilated in a geriatric patient?

A
  • upper lung is better ventilated
  • lower lung is better perfused
  • resulting in a V/Q mismatch
58
Q

How do blood gases change with normal aging? How does patient sensitivity to these change?

A
  • PaO2 usually decreases but PaCO2 usually does not change with age
  • patients become less sensitivity to both hypoxia and hypercapnia
59
Q

What renal features decline with age?

A
  • number of functioning glomeruli
  • renal mass
  • creatinine clearance
60
Q

What is normal creatinine clearance at ages 60 and 90?

A
  • about 90 mL/min in those that are 60 y.o.

- about 60 mL/min in those that are 90 y.o.

61
Q

How are geriatric drugs dosed?

A

according to GFR

62
Q

How do we correct CrCl in geriatric patients?

A

CrCl = [(140-age) x lean body weight] / (72 x serum creatinine)

multiply by 0.85 if it is a women

estimate LBW as:

  • men = 50 + 2.3 x inches over 5 ft
  • women = 45.5 + 2.3 x inches over 5 ft
63
Q

Why is NPO after midnight dangerous for geriatric patients?

A

because they lose the ability to maximally conserve water in response to water-deprived or hyperosmolar conditions

64
Q

Why do geriatric patients often have lower blood volume?

A
  • reduced thirst
  • less lean mass (impacts TBW)
  • reduced renin response to volume depletion
  • ANP may be increased, inhibiting aldosterone release
65
Q

What is the most common endocrine disorder in the elderly?

A

hypothyroidism

66
Q

Why are geriatric patients more susceptible to TB?

A

because with reduced immune response, they can get a reactivation

67
Q

Geriatric patients have a reduced incidence of what group of diseases?

A

autoimmune disease

68
Q

What is a normal height loss during the aging process?

A

two inches by age 80

69
Q

What is the critical feature to be aware of when testing deep tendon reflexes in the elderly?

A

the key is too look for symmetry because some reflexes may be absent due to normal aging

70
Q

How do neurologic changes affect the way you take a history with geriatric patients?

A

slowed information processing should mean that you take a history at a slower pace

71
Q

How does acute mental status change with normal aging?

A

acute mental status change is never normal

72
Q

What changes are seen in those with “atrophy consistent with age”?

A
  • enlarged subarachnoid space
  • narrower gyri
  • wider sulci
  • enlarged ventricles
73
Q

What is considered poly pharmacy?

A

more than five prescriptions

74
Q

Which patients are at greater risk of poly pharmacy?

A
  • over 85
  • caucasian
  • educated
  • CrCl less than 50
  • BMI less than 20
  • insured
75
Q

Why does absorption of an oral drug change in the elderly?

A
  • slowed gastric emptying
  • reduced gastric acid output
  • decreased intestinal motility, blood flow, and surface area
76
Q

What is the net affect of aging on GI absorption of a drug?

A

there is no significant change in quantity absorbed but the time to onset or peak may be delayed

77
Q

Why does distribution of a drug change in the elderly?

A
  • they have more body fat but less muscle mass and body water
  • they have decreased cardiac output and altered regional blood flow
78
Q

What is the net affect of aging on drug distribution?

A
  • the volume of distribution of lipid soluble medications increases
  • the volume of distribution of water soluble medications decreases
  • and changes in Vd affect loading dose and half-life
79
Q

Why do changes in the volume of distribution of a drug impact other drug parameters in the elderly?

A

because Vd affects the necessary loading dose and the half-life

80
Q

What protein binding changes in the elderly affect drug pharmacokinetics?

A
  • they have decreased serum albumin and decreased protein affinity
  • there is also an increase in a1-acid glycoprotein
  • as a result, many protein-bound drugs have an increased free fraction in the elderly
81
Q

Which is more significant in the elderly, changes in volume of distribution of plasma protein binding?

A

in most cases, Vd is more significant

82
Q

How does hepatic function change with normal aging?

A
  • decreased hepatic mass

- decreased hepatic blood flow

83
Q

Which liver metabolism pathways are affected by normal aging?

A
  • phase 1 is diminished
  • phase 2 is unchanged
  • CYP450 activity is unchanged
84
Q

How do changes in hepatic metabolism of drugs alter our drug selection?

A
  • since phase 1 is impaired, prodrugs are not activated as well
  • we try to use drugs that rely only on phase 2 reactions because these have more predictable effects
85
Q

Which benzodiazepines are preferred in elderly patients? Why?

A

we prefer temazepam, oxazepam, and lorazepam because these relay only on phase 2 metabolism by the liver, which is relatively unaffected by normal aging

86
Q

How does renal elimination of drugs change with normal aging?

A
  • there is decreased renal blood flow and tubular secretion
87
Q

Why can’t serum creatinine be used as a good estimate of GFR in elderly patients?

A
  • because it remains stable while GFR declines

- it remains stable because there is a reduction in muscle mass with age

88
Q

How do we estimate lean body weight for geriatric patients?

A
  • men = 50 + 2.3 x inches over 5 ft

- women = 45.5 + 2.3 x inches over 5 ft

89
Q

What consensus was recently formed regarding PO dosing based on renal function?

A

found 10 meds to be avoided if CrCl is <30mL/min
- chlorpropamide, colchicine, cotrimoxazole, glyburide, meperidine, nitrofurantoin, probenecid, propoxyphene, spironolactone, triamterene
found 8 meds to be used with caution or at lower doses in such patients
- acyclovir, valacyclovir, ranitidine, rimantidine, ciprofloxacin, gabapentin, memantine, amantadine

90
Q

Which displays more interpersonal variation, geriatric changes in pharmacokinetics or pharmacodynamics?

A

pharmacokinetics are more consistent and less variable

91
Q

What three types of pharmacodynamic changes are seen in geriatric patients?

A
  • numbers of receptors (e.g benzodiazepines)
  • sensitivity of receptors (e.g. beta-adrenergic receptors)
  • counter regulatory mechanisms (e.g. decrease in baroreceptor sensitivity)
92
Q

How do the pharmacodynamics of warfarin change in geriatric populations?

A

there is increased sensitivity and a narrower therapeutic index

93
Q

How do the pharmacodynamics of anticholinergics change in geriatric populations?

A

there is increased sensitivity

94
Q

What side effect is more likely in geriatric patients taking antipsychotics?

A

tardive dyskinesia and parkinsonism

95
Q

Why are geriatric patients more susceptible to digoxin toxicity?

A

because they have increased sensitivity of Na/K-ATPase

96
Q

How are geriatric patients likely to respond to ACE inhibitors compared to younger populations?

A

because they already have decreased renin and aldosterone levels, they are likely to have a decreased response to ACE inhibitors

97
Q

What are four categories of medication-related problems?

A
  • untreated indication
  • drug interaction
  • adverse drug reaction
  • improper drug selection
98
Q

What is meant by the “untreated indication” medication-related problem in the elderly?

A

often there is a fear of adding one more drug to a growing list in geriatric patients, leading some conditions untreated

99
Q

What are some common untreated indication examples in the elderly?

A
  • depression in the nursing home
  • osteoporosis in the nursing home
  • atrial fibrillation/anticoagulation
  • hypertension
  • MI primary or secondary prevention
  • opioids for fear of addiction
100
Q

What are the START/STOPP criteria?

A
  • a screening tool used to analyze a patients drug list
  • START are drugs you may be falling short with by not starting therapy
  • STOPP are drugs that may be inappropriate and should be removed
101
Q

What are some examples of START drugs?

A
  • anti-coagulation with afib
  • statin therapy
  • vitamin D in those with known OP
102
Q

What are some examples of STOPP drugs?

A
  • duplicate prescriptions
  • loop diuretics for HTN or dependent ankle edema only
  • first generation antihistamines
  • long-term BZD use
  • PPU use for uncomplicated PUD
  • long-term NSAID use for mild OA
103
Q

Which drugs are most likely to have DDIs?

A
  • highly protein bound drugs
  • those metabolized by CYP 450
  • inducers/inhibitors of CYP
104
Q

What are the five most common DDIs and their results in the elderly?

A

mostly cardiovascular/antihypertensive and CNS/psychotropic combinations

  • ACE inhibitor + diuretic: hypotension, hyperkalemia
  • ACE inhibitor + potassium: hyperkalemia
  • anti-arrhythmic + dirutic: electrolyte imbalance, arrhythmia
  • BZD + antidepressant: confusion, sedation, falls
  • BZD + antipsychotic: confusion, sedation, falls
105
Q

What are five risk factors for adverse drug reactions in the elderly?

A
  • polypharmacy
  • female gender
  • small body size
  • hepatic/renal insufficiency
  • pervious ADRs
106
Q

If an elderly patient presents with a new symptom, what should be your first consideration?

A

that it might be a side effect of another drug they are on

107
Q

What is a prescribing cascade?

A

the idea that a patient starts a drug and a while later develops an adverse drug effect, which is not recognized as such; instead, the doctor prescribes a different medication, which has it’s own side effect that is treated by a third drug and so on

108
Q

What are the Beers criteria used for?

A
  • used to improve the care of older adults by reducing their exposure to potentially inappropriate medications
  • it is used as a drug-selection tool
109
Q

The Beers criteria divide drugs into what three groups?

A
  • avoid in older adults regardless of disease
  • potentially inappropriate when used in older adults with a specific condition
  • used with caution
110
Q

What are the two major limitations of the Beers criteria?

A
  • assumes medications with high risk of side effects in the elderly actually will cause the ADR in all
  • does not address inappropriate use of an appropriate medication
111
Q

What is the medication appropriateness index?

A

a set of 10 questions used to review each medication on a patients drug list

112
Q

What are the limitations of the medication appropriateness index?

A
  • it is time consuming

- it does not fully identify underuse

113
Q

What questions are asked on the medication appropriateness index?

A
  • is there an indication for the drug
  • is the med effective for the condition
  • is the dosage correct
  • are the directions correct
  • are the directions practical
  • are there significant DDIs
  • are there significant drug-disease interactions
  • is there unnecessary therapeutic duplication
  • is the duration of therapy acceptable
  • is this drug the least expensive compared to others of equal utility
  • is the drug being appropriately taken
  • are therapeutic endpoints being monitored
  • are there possible adverse drug reactions occurring
114
Q
  • List ten PIRX older adults should avoid or use with caution?
A
  • NSAIDs
  • digoxin
  • certain diabetes drugs
  • muscle relaxants
  • certain anxiety/insomnia meds
  • certain anticholinergics
  • meperidone (demerol)
  • ORC combination products containing anticholinergics
  • antipsychotics
  • estrogen
115
Q

What are the mediators of cellular aging?

A

DNA damage, replicative senscence, and misfiled proteins

  • ROS-mediated DNA damage
  • telomere shortening inhibits cellular replication
  • defective protein homeostasis leads to misfolding, deposition, and impaired cell functioning
116
Q

What is the only mechanisms that appears to counteract aging?

A

the nutrient sensing pathway, which upregulates DNA repair and protein

117
Q

What is the genetic theory of aging?

A

sporadic genetic errors, due to ROS or defective DNA repair gradually accumulate with age

118
Q

What is the cellular senescence theory of aging?

A

the idea that telomere attrition contributes to cellular aging as set by the Hayflick limit

119
Q

Which theory of aging is accepted most widely?

A

cellular senescence

120
Q

What group of proteins mediate the nutrient sensing pathway that counteracts aging?

A

altered sirtuin proteins

121
Q

What is Werner syndrome?

A
  • a syndrome of premature aging associated with defective DNA helicase
  • causes rapid accumulation of chromosomal damage that is thought to mimic the injury that normally accumulates during cellular aging
122
Q

What is replicative senescence?

A

a terminally non-dividing state arrived at after a normal cell has reached it’s maximum number of divisions

123
Q

What two mechanisms appear to control replicative senescence?

A
  • telomere attrition

- activation of tumor suppressor genes, particularly those at the CDKN2A locus

124
Q

What is the physiologic importance of the CDKN2A locus of tumor suppressor genes?

A

this locus is believed to be up-regulated to mediate replicative senescence in normal cells

125
Q

How do cancer cells appear to avoid replicative senescence?

A

they re-express or up-regulate telomerase, to lengthen telomeres and put off attrition

126
Q

What are the two mechanisms that maintain protein homeostasis?

A
  • chaperones maintain proteins in their correctly folded conformations
  • degradation of misfolded proteins by the autophagy-lysosome and ubiquitin-proteasome systems
127
Q

Is cellular senescence followed by necrosis or apoptosis?

A

apoptosis

128
Q

What behavior modification has been shown to prolong lifespan in animal models?

A

caloric restriction

129
Q

Sirtuins mediate what effects?

A

anti-aging by inhibiting metabolic activity, reducing apoptosis, stimulating protein folding, and inhibiting the harmful effects of ROS

130
Q

How is it thought that caloric restriction prolongs life?

A
  • increasing sirtuins

- reducing IGF-1 activity, which lowers the rate of cell growth and metabolism and reduces cellular damage

131
Q

What are the seven types of DNA lesions?

A
  • telomere shortening
  • base damaage
  • adduct formation
  • interstrand crosslink
  • spindle errors
  • double-strand break
  • mismatch
132
Q

What are the “9 mechanisms of aging”?

A
  • primary hallmarks (causes of damage): genomic instability, telomere attrition, epigenetic alteration, and loss of proteostasis
  • antagonistic hallmarks (responses to damage): de-regulated nutrient sensing, mitochondria dysfunction, cellular senescence
  • integrative hallmarks (culprits of the phenotype): stem cell exhaustion, altered intercellular communication
133
Q

When running out DNA on a gel, how does that from whole cells, necrotic cells, and apoptotic cells compare?

A
  • whole cells remain near the loading well (large, intact)
  • necrotic create a smear pattern as DNA is broken down into randomly sized fragments
  • apoptotic create a ladder as DNA is systematically chopped up
134
Q

What is lipofuscin?

A
  • a pigment found in aged cells that is a product of per oxidation of fatty acids
  • thought of as a “wear and tear” pigment
  • doesn’t appear to negatively impact cellular function
135
Q

What is platelet rich plasma? What is it’s clinical benefit and use?

A
  • an injection of the patient’s activated platelets
  • theorized that their release of PDGF stimulates repair
  • clinical trials don’t support it’s use
136
Q

What is the central dogma of pathology?

A

molecular damage leads to cell damage and then to organ dysfunction which presents as a constellation of clinical symptoms that we classify as a disease

137
Q

Chronic, non-lethal cellular injury leads to what changes?

A

atrophy, hypertrophy, dysplasia, etc.

IC 1.0 (24 decks)

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