Geriatrics Flashcards

1
Q

What % of the population is over 65 in 2030 and 2050

A

By 2030, 20% of US > 65 y/o

By 2050, 2 billion people worldwide over 60 y/o

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2
Q

What is aging (4)

A

Universal and progressive physiologic process

Decreasing end-organ reserve
Decreased functional capacity
Increased homeostatic imbalance
Increasing incidence of pathophysiologic processes

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3
Q

Memory and aging

A

Memory decline
40% of people > 60 y/o have some sort of memory decline

Not inevitable
Relates to ability to complete ADL’s

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4
Q

NS structure changes with aging

A

Cerebral atrophy; brain size shrinks. White matter shrinks more than gray matter. Don’t loose neurons but we lose functioning

Decrease grey matter;
Neuronal shrinkage (only a small neuron loss)

Decrease white matter;
Increases in ventricular size between the atrophy and decreases in gray/white matter leads to-> Progressive loss of memory, balance, mobility

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5
Q

NS and aging changes with nerve transmission

A

of synapses or amount of neurotransmitters decrease/ don’t work aswell because in decrease in number of synapses or a decrease in nt release or decrease amount built.

Animal studies;
Significant decrease in Dopamine, Ach, norepi and serotonin (all not)
No change in glutamate
Coupling of CMRO2, CBF, EEG unchanged

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6
Q

Neuraxial changes with Aging

A

Decreased epidural space

Increased permeability of dura

Decreased volume of CSF

Decreased diameter/number of myelinated fibers in dorsal and ventral nerve roots

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7
Q

Peripheral nervous system changes with aging

A

Inter-Schwann cell distance decreased

Conduction velocity decreased

Elderly more sensitive to Neuraxial blocks and Peripheral nerve blocks

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8
Q

Cardiac changes with aging (8)

A

Myocyte number decreases

LV wall thickens

SA node cells decrease

Conduction velocity decrease

Thickened and calcific aortic valve

Decreased contractility

Increased ventricular stiffness…higher filling pressure

Less Beta-adrenergic sensitivity

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9
Q

Tachy/brady syndrome

A

SA node cells decrease; don’t have as regular rhythm= more susceptible to a fib or brady tachy syndrome where the SA node doesntk now how to be regular so it speeds up and then slows down; put on Beta blocker to keep tachycardia at bay and they will have a pacemaker inserted for safety baselin.

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10
Q

Response of decrease beta adrenergic sensitivity

A

↓ maximal heart rate and ejection fraction during stress= decreased max rate

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11
Q

Vessel changes with aging

A

Vascular stiffness;
Due to Breakdown of collagen and elastin
Less NO related vasodilation; cant stretch and bound back
Early wave deflection…increased afterload, diastolic dysfunction

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12
Q

What is early wave deflection

A

As stroke volume is ejected = have arterial wave to periphery and to return back to the heart because of increased afterload it causes some diastolic dysfunction = stiff vessels that cant relax and we get the wave deflected back to the heart.

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13
Q

Pulmonary-Structural chagnes with aging

A

Loss of elastic recoil and loss of surfactant

Enlarged bronchioles and alveolar ducts
Early collapse of small airways during exhalation

Loss of vertebral height and calcification of vertebra

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14
Q

Loss of elastic recoil and loss of surfactant results in ……

A

Increased lung compliance

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15
Q

Enlarged bronchioles and alveolar ducts
Early collapse of small airways during exhalation causes……(3)

A

Increased anatomic dead space
Increased closing capacity
Impaired gas exchange

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16
Q

Loss of vertebral height and calcification of vertebra results in…..

A

Barrel chest
Diaphragmatic flattening
Chest wall stiffness….increased work of breathing

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17
Q

Changes to pulmonary function with aging
Decrease fev 1 by……

A

total lung capacity about the same

↓ vital capacity
↑ closing capacity
↑ residual volume

Decrease muscle mass and ↑ closing capacity
Decrease FEV1 by 6-8% per decade

Weaker pharyngeal muscles

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18
Q

Weaker pharyngeal muscles results in …….. (4)

A

Decreased clearance of secretions
Less efficient coughing
Decreased esophageal motility
Less protective upper airway reflexes

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19
Q

VQ matching with aging

A

Relationship between FRC and closing capacity;
Mismatch increases
Most important MOA for alveolar-arterial oxygen gradient
Shunt increases , arterial oxygenation declines

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20
Q

Renal changes with aging

A

GFR decreases;
Comorbidities may exacerbate. less IVP dye excretion

Blunted responses to aldosterone, vasopressin, renin;
Trouble adjusting Fluid &Electrolyte

Retention and UTI’s more common; difficult to contract because of decreased muscle

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21
Q

GI and Hepatic changes with aging

A

Liver function declines

Less PONV!
Avoid prochlorperazine, promethazine, metoclopramide (because of increased sensitivity to side effects)

22
Q

What medications are okay and not okay for an aged liver

A

drugs that have Phase I metabolism are not OK… (oxidation, reduction, hydrolysis via CYP450)

drugs that use Phase II metabolism are OK…(acetylation and conjugation)

23
Q

muscloskeletal changes with aging (4)

A

Muscle mass and strength declines

Subcutaneous fat thins

Impaired wound healing

Osteoarthritis

24
Q

Thermoregulation changes with aging

A

Vasoconstriction threshold
Comparable in infants, children, adults/ elderly are likely to be 1 degree C less for adults 60-80 y/o

25
Q

Operative risks with elderly

A

Ideas;
high mortality 90 y/o and up
ASA status predicted mortality (>4)

uncorrectable comorbidity in SICU; 100% mortality

high mortality from nursing home residents

26
Q

Significant Predictors of 6 month-1 year Mortality (6)

A

Impaired cognition

Recent fall

Hypoalbuminemia

Anemia

Functional dependence

Comorbidities

27
Q

surgery and anesthesia on vulnerable brain

A

Surgery and anesthesia causes peripheral inflammatory response crosses BBB and results in neuro inflammatory response = release of pro inflammatory mediators and in normal and healthy brain; the body takes care of the TNF/ WBC/ Interleukin and may have short term cognitive decline and may not be as sharp for a few days but you get over it and go back to normal.

If we have a neuroinflammatory releases of mediators to a vulnerable brain then that causes a greater anti inflammatory response / greater release of the mediators and the body cant recover from = long term cognitive decline.

28
Q

Neurotoxicity Factors

A

Amyloid β
Tau
Calcium
Neuroinflammation (TNF, interleukin)

29
Q

Anesthesia and Amyloid β

A

First studied with Halothane/mice

Significant increases in amyloid plaque

Young mice had improvement in learning/memory

Old mice accelerated onset of AD

… unclear translation to humans; other factors clearly involved

29
Q

Amyloid-β

A

Fragment of synaptic origin

Unknown function

Accumulates extracellularly to form plaques
Originally thought to be toxic
Now? Less so…labile…aggregate then eliminated
Plaques May disrupt cell membranes over time

30
Q

Tau

A

Neurofibrillary tangle (NFT);
Phosphorylated and aggregated 𝜏 protein

Destabilizes microtubules; Tau can be aggregated to large chunks that destabilizes microtubules in the cells so they don’t function as well.

Decreases in temperature 2-3 degrees C increases amount of 𝜏
(tauopathy)

Repeated exposure to Halothane, Isoflurane, Sevoflurane;
Increased phosphorylated 𝜏

31
Q

Relationship of Amyloid and Tau to Symptoms

A

Both increase cognitive impairment the more accumulation you have

32
Q

Calcium Release and Anesthesia and dantrolene

A

Exaggerated release from endoplasmic reticulum; Specifically ryanodine and IP3 receptors

Volatile anesthetics; known to cause malignant hyperpyrexia
Less dramatic release causing neurotoxicity???
Inhibition of release delay/decrease neurotoxicity???

Dantrolene;
Doesn’t cross BBB; so wont treat neurotoxicity/ confusion
Significant skeletal muscle weakness

33
Q

Neuroinflammation mediators and modulators

A

Contributes to cognitive decline Through release of inflammatory factors
Cytokines
IL-6
TNF⍺

some Anesthesia drugs capable of modulating inflammation; dexamethasone, lidocaine, toradol

34
Q

Anesthesia and the brain

A

General anesthetics alter cognitive state While they are in CNS

Alteration outlasts surgery
Depends on drug, duration of exposure and magnitude of exposure;
causes of cognitive decline;
Isoflurane > Desflurane > Propofol

35
Q

Risk factors for cognitive decline with anesthesia

A

Increasing age,
duration of anesthesia, lesser education,
a second operation,
postoperative infection and
respiratory complications….

36
Q

Anesthesia Implications for elderly (7)

A
  1. Using neuraxial/regional anesthesia when possible
  2. Avoid long-acting NMBD and reverse adequately
  3. Opioid sparing strategies
  4. Neutralization of stomach acid with non-particulants
  5. Consider using EEG based titration
  6. Avoid hypotension
  7. Pad skin and nerves
37
Q

Goal Bis for elderly

A

60

38
Q

Drug Challenges r/t Heart in the elderly

A

⬇️ Cardiac Output;
slower distribution to initial site of action
slower redistribution
slower distribution to metabolic organs

39
Q

Drug Challenges r/t Neuromuscular Junction in elderly

A

⬆️ distance between axon and motor end plate
⬇️ concentration of Ach receptors
⬇️ amount of Ach in presynaptic vesicle
⬇️ release of Ach upon neuronal impulse

40
Q

Kidney/Liver Dependent Metabolism vs Not

A

Kidney/Liver dependent metabolism drugs causes;
Prolongation of effect
Decreased need during maintenance phase
Delayed recovery phase for non-depolarizers

Not kidney/liver dependent causes;
No significant prolongation of effect
Essentially same requirements during maintenance
Essentially no delay in recovery phase

41
Q

Pulmonary Resection in elderly mortality rate

A

Mortality 80-92 y/o 3%

Lobectomy mortality acceptable
Pneumonectomy mortality excessive

42
Q

Pulmonary resection and respiratory and cardiac complications in elderly compared to younger pop

A

Respiratory complications 40% (2x younger pop.)

Cardiac complications 40% (3x younger pop.)

43
Q

Predicted Postoperative FEV1 with lung resection

A

ppoFEV1 = Preop FEV1 % x (1-% lung tissue removed/100)

R lung and L llung segments (42)
R; 6,4,12
L; 10, 10

44
Q

Algorithm for Preoperative Assessment:Thoracic (non-cardiac) Surgery

A

Tee to rule out Pulm htn-> exercise tolerance?-> perfusion scan? Echo? Coronary angiography

45
Q

Three legged stool of prethoractomy respiratory assessment

A

Respiraotry mechanics; FEV1 (ppo >40%)
MVV, RV/TLC, FVC

Cardiopulmonary reserve;
VO2max (>15 ml/kg/min)
Stair climb > two flights, 6 min walk.
Exercise SpOx <4%

Lung parenchymal function;
DLCO
(PPO >40%)
PaO2 >60
PaCo2<45

46
Q

PPO FEV1 >40% post thoracotomy

A

Extubate in OR if pt awake alert, warm and comfortable

47
Q

PPO FEV1 30-40% post thoracotomy

A

Consider extubation beased on;
exercise tolerance
DLCO
VQ scan
Associated dz

48
Q

PPO FEV1 <30% post thoracotomy

A

staged weaning for mech, ventilation consider extubation if >20% plus; thoracic epidural analgesia

49
Q

What is Postoperative Cognitive Dysfunction (POCD)?

A

An objectively measured decline in cognitive function that persists beyond the period expected