Diabetes Flashcards

1
Q

4 types of diabetes

A
  • Type I Diabetes*
  • Type II Diabetes*
  • Gestational Diabetes
  • Maturity-Onset Diabetes of the Young
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2
Q

definition of diabetes

A

=Chronic, complex disorder with impaired nutrient metabolism (glucose).
-Main feature is impaired glucose regulation (hyperglycemia).

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3
Q

= Chronic hyperglycemia that results from issues with glucose regulation manifested by
◦ Reduced insulin secretion
◦ Reduced insulin function

A

Diabetes Mellitus

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4
Q

Viral infections can be a trigger for what type of Diabetes?

A

Type 1

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5
Q

Type of Diabetes that is autoimmune with beta cells destroyed

A

Type 1

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6
Q

Type 1 diabetes results in _______ insulin secretion

A

decrease

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7
Q

Type 1 Diabetes Patho

A
  • Cells cannot use glucose
  • Onset: Sudden
  • Glucose builds up in blood b/c no insulin to carry it in
  • Back up mechanism: Break down of fat and protein (Lipolysis & proteolysis) as energy source
  • Increased ketogenesis (breakdown of fat) –> ketone bodies
  • Increased release of counter-regulatory hormones
  • Glucagon —> causes more glucose release
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8
Q

Polyuria and Diabetes- What happens to K levels?

A

‣ Loss of electrolytes- overall K is low but it looks high

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9
Q

3 things that are happening b/c of polyuria

A

‣ Loss of glucose in urine
‣ Loss of electrolytes- overall K is low but it looks high
‣ Loss of water

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10
Q

3 things Dehydration in Type I leads to ….

A
  • Hypovolemia
  • Hypoxia –> Ischemic tissue –> Lactic acid production (due to anaerobic)—>
  • Metabolic acidosis
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11
Q

WTF is ketogenesis

A

• Conversion of fat to ketone bodies
◦ Acetone, Acetoacetate, B-hydroxybutyrate
• Metabolic acidosis

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12
Q

How does body try to fix metabolic acidosis from Type 1 DM ketogenesis ?

A

-Metabolic acidosis yields an attempt by the lungs to correct the acidosis
-We need to blow off some CO2 & acid
• Increased rate of breathing
• Increased depth of breathing
• Kussmaul breathing- rest alkalosis

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13
Q

Hallmark sign of acidosis related to hyperglycemia =

A

kussmaul breathing

• Increased rate and depth of breathing

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14
Q

What is type II DM? What’s up with insulin, beta cells? How?

A

• Insulin resistance, progresses to decreased beta cell secretion.
• Decreased insulin secretion.
◦ Pancreas responds to decreased insulin sensitivity by developing more insulin
◦ Eventually, the beta cells can no longer produce as much insulin
◦ =Less insulin production

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15
Q

Metabolic syndrome has strong correlation with Type 1 or Type 2 DM?

A

Type 2

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16
Q

when do we see onset of Type 2 DM?

A

in 50’s ….becoming more common in youth

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17
Q

If you have gestational diabetes you are more likely to develop….

A

type 2 DM

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18
Q

Islet Cells: Alpha vs Beta, what is the difference?

A

◦ Alpha ->Secrete glucagon

◦ Beta->Produce insulin and amylin

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19
Q

Glucagon vs Insulin, whats the difference?

A
  • Glucagon triggers a release of glucose from the liver and skeletal muscle.
  • Insulin, secreted with food intake, moves glucose from blood into cells (energy).
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20
Q

Insulin keeps blood glucose and _____ levels in normal range

A

lipid

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21
Q

Where does insulin get converted into a usable hormone?

A

in the liver

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22
Q

_____ is the key that helps the glucose get inside the cell

A

Insulin

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23
Q

In the liver, insulin does 6 things. What are they?

A
  • Suppresses production of glucose
  • Promotes production and storage of glycogen
  • Inhibits glycogen breakdown into glucose
  • Inhibits conversion of fats to acids and proteins to glucose
  • Manufactures glucose from glycogen (GLYCOGENOLYSIS)
  • Manufactures glucose from amino acids, waste products and fat byproducts (GLUCONEOGENESIS).

This all means: Insulin and liver KEEP BLOOD GLUCOSE LEVELS WHERE THEY NEED TO BE

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24
Q

Gluconeogenesis vs glycogenolysis ….taking ya back to A&P with this question

A
GLYCOGENOLYSIS= glucose made from glycogen 
GLUCONEOGENESIS= glucose made from amino acids, waste products and fat byproducts
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25
Q

Insulin does 2 things in the muscle, what are they?

A
  • Stimulates glucose uptake

* Promotes protein and glycogen synthesis

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26
Q

In fat cells insulin does 1 thing, what is it?

A

• Promotes triglyceride storage

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27
Q

Basal VS Prandial Insulin secretion

A

Basal = insulin is secreted continuously throughout day (fasting).
Prandial = insulin secreted after eating.
◦ Initial burst within 10 minutes of eating

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28
Q

Normal blood glucose range

A

60-100mg/dL

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29
Q

Glucose is stored as _____ in the liver and ___ ____ ____ in other tissue

A

glycogen, free fatty acid (aka triglycerides?)

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30
Q

What does glucagon trigger?

A

= Counteracts insulin—>Triggers conversion of glycogen to glucose in liver and muscle whenever we need it

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31
Q

name 3 other hormones besides glucagon that help increase glucose

A

◦ Epinephrine
◦ Norepinephrine
◦ Cortisol

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32
Q

Which drug class prevents counter regulatory methods and makes it hard to tell if they have low CBG ?

A

Beta blockers

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33
Q

WTF are incretins , what do they do?

A
Incretin hormones = secrete in response to eating.  
• Increase insulin secretion 
• Decrease glucagon secretion
• Slow gastric emptying (gastroparesis) 
• Prevents hyperglycemia after meals
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34
Q

If you have no insulin you have (2)….

A

◦ No insulin=No cellular energy

◦ No insulin=glucose building up in blood (hyperglycemia)

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35
Q

Without insulin, the body will break down stored _____ and _____ to make energy and use hormones to make glucose.
–> The breaking down of fat creates ketones bodies to form in the blood.

A

fat and protein

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36
Q

Characteristics of metabolic syndrome

A
  • Presence of metabolic factors that increase risk for developing type II diabetes.
  • Waist circumference (>40 in men, >35 in women)
  • Fasting blood sugar >100
  • Triglyceride levels >150, HDL <40.
  • Hypertension
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37
Q

3 p’s of diabetes

A

• Polyuria- Excessive urination rapid onset
◦ Osmotic diuresis from excessive glucose in urine
• Polydipsia- Excessive thirst rapid onset
◦ Secondary to polyuria and dehydration
• Polyphagia- Excessive hunger rapid onset
◦ “cell starvation” due to insulin not moving glucose into cells

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38
Q

complications of type 2 DM

A
• Dehydration
• Electrolyte imbalances
• Vascular changes->  Organ Dysfunction
	◦ Microvascular or Macrovascular
• Neuropathies
• Decreased immune response
• Poor wound healing
• Acid-Base imbalances
• Early Mortality
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39
Q

Lets talk more about K levels- loss of K in urine leads to hypokalemia. During acidosis something else happens though….

A

Hyperkalemia!

◦ During acidosis, potassium moves out of cells into the blood (hyperkalemia) and switches place H+ ion
◦ When we correct the acidosis, potassium moves back into the cell (normal or hypokalemia)

◦ When we correct the acidosis, potassium moves back into the cell = normal or hypokalemia
◦ If fix acidosis too quickly then we can send K too low to quickly

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40
Q

We need to fix acidosis slowly to prevent causing ____

A

hypokalemia

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41
Q

you can also have what other electrolyte change with Diabetes?

A

hypo or hypernatremia

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42
Q

Vascular changes in diabetes occur secondary to

A

hyperglycemia

–causing thickening to basement membranes, glucose toxicity, chronic ischemia of small vessels, and tissue hypoxia.

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43
Q

Macrovascular changes associate with Diabetes

A

Cardiovascular disease, Cerebrovascular disease, peripheral vascular disease

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44
Q

Microvasular changed associated with Diabetes?

A

Nephropathy, neuropathy, retinopathy

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45
Q

How does hyperglycemia cause kidney disease? Whats the patho?

A

◦ Hyperglycemia > increased pressure in kidney > increased perfusion causes vessels to leak > decreasing kidney oxygenation> ischemia> CKD.

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46
Q

How does hyperglycemia cause peripheral neuropathy?

A

• Vessel changes secondary to hyperglycemia leading to decreased tissue perfusion and poor nerve impulses. Excess glucose collects in nerves and impairs motor nerve conduction.

47
Q

Is peripheral neuropathy from diabetes reversible?

A

nope! it is irreversible damage

48
Q

Peripheral Neuropathy from diabetes can lead to system wide problems like….

A
‣ Foot Injury (Late complication)
		‣ Skin
		‣ Gastrointestinal
		‣ Neurogenic bladder
		‣ Erectile dysfunction
49
Q

How does the damage from peripheral neuropathy first present? and later?

A

• Damage starts as pain and progresses to sensation loss.

50
Q

Can diabetes cause autonomic neuropathy?

A

Yes!

51
Q

Examples of disease development of autonomic neuropathy from diabetes?

A
  • Dysfunction of the nerves that regulate the involuntary body functions.
  • Sympathetic and Parasympathetic nerves
  • Urinary retention, orthostatic hypotension, syncope, gastroparesis, tachycardia, exercise intolerance, sexual dysfunction,…
52
Q

Where do we see motor neuropathy due to diabetes? how does it manifest?

A
  • Dysfunction of body’s motor nerves.
  • Typically occurs in longer nerves (i.e spine to feet).
  • Weakness, droop, cramping, twitching, atrophy,…
53
Q

Charcot foot-what causes it , what does it affect, what does it look like?

A
  • a complication of peripheral neuropathy in diabetics.
  • affect the bones, joints, and soft tissues of the foot or ankle.
  • Combination of bone disintegration and trauma can alter and deform the shape of foot/ankle.
54
Q

Prolonged wound heal on feet put diabetics at risk for

A

INFECTION

55
Q

3 ways to help save kidneys from damage due to DM

A

◦ Optimal glucose control
◦ Kidney protective medications
◦ Blood pressure control

56
Q

Once albuminuria is present focus on preventing progression by…

A

‣ BP control
‣ Glucose control
‣ Avoid nephrotoxic agents

57
Q

if you have type 1 DM do albuminuria test when?

A

after 5 years since diagnosis

58
Q

retinopathy prevention for diabetics

A

◦ Control of blood pressure
◦ Control of hyperglycemia
◦ Control of lipids
◦ Annual eye exams

asymptomatic until vision loss occurs

59
Q

Hypogylcemia = CBG < ____

A

70

60
Q

Coma can occur when CBG < ____

A

50

61
Q

DKA- type 1 or Type 2?

A

Type 1

62
Q

CBG for DKA will be >

A

◦ CBG >250(>300 for Messer lecture)

63
Q

quick patho of DKA

A

• Uncontrolled hyperglycemia, insulin deficiency > Body breaks down fat for energy> Ketones increase in blood > pH decreases (acidosis).

64
Q

s/s of DKA

A
  • Classic 3 P’s
  • Rotten, fruity breath (ketones)
  • Nausea/vomiting
  • Abdominal pain
  • Dehydration
  • Weakness
  • Shock
  • AMS, up to coma.
65
Q

Assessment for DKA

A

• Respiratory status
◦ Rate, pattern, depth, accessory muscle, breath smell…
• LOC
• Hydration
• Skin turgor, Skin temperature, mucous membranes, urine output and color, JVD…
• Labs
◦ Blood glucose, sodium, bicarb, potassium, anion gap, osmolality, ABG,….
• Vital signs
◦ Pulse, hypotension…
• ROM/Strength
◦ Weakness

66
Q

DKA interventions

A
  • IVF : NS for CBG >250, then D5 1/2NS (may include KCl-) once CBG <250.
  • IV drip Regular Insulin
  • Sodium bicarb drip, if severe acidosis pH<7.0 and bicarb <5.
  • Oral intake of fluids
67
Q

Hyperosmolar Hyperglycemic State (HHS), type 1 or type 2?

A

type 2

68
Q

Hyperosmolar Hyperglycemic State (HHS)- does this have ketones?

A

NO. DKA is your ketone dude

69
Q

onset for HHS vs dka?

A
HHS= gradual 
DKA = sudden
70
Q

higher morbidity- HHS or DKA?

A

HHS

71
Q

What happens to cause HHS?

A

• Increase in blood osmolarity due to insulin deficiency and hyperglycemia.

72
Q

do you have acidosis with HHS?

A

NOPE

73
Q

S/S of HHS

A
  • Classic 3 P’s
  • Profound Dehydration
  • Weight loss
  • Dry skin
  • Lethargy, can progress to coma
74
Q

Contributing factors to HHS

A

MI, Sepsis, pancreatitis, stroke, medications (diuretics, corticosteroids, Ca channel blockers, beta blockers…)

75
Q

Assessment for HHS

A

• LOC
• Hydration
• Skin turgor, Skin temperature, mucous membranes, urine output and color, JVD…
• Labs
◦ Blood glucose, osmolality, sodium, BUN, Creatinine, ABG (pH will be >7.3), serum bicarb, WBC…
• Vital signs
◦ Pulse, hypotension, fever, respiratory rate…

76
Q

HHS interventions?

A
  • IVF of 1/2 NS or NS = SLOW process to avoid too rapid changes in osmolarity.
  • Requires close monitoring of serum osmolality
  • Once CBG is <250-300, NS may be changed out for a dextrose containing fluid.
  • May require potassium replacement for hypokalemia
  • IV drip regular insulin
77
Q

A1C > ____ = diagnostic

A

6.5

78
Q

A1C > ____ = indicative of poor DM control

A

8%

79
Q

A1C ______ = increased risk of developing DM

A

5.7-6.4%

80
Q

fasting vs non fasting CBG for diagnosing DM?

A
  • fasting BS >126 (normal is 80-110 or <100) on >2 occasions

* non-fasting BS >200

81
Q

Glucose tolerance > ____ = diagnosis of DM

A

> 200

normal is <140

82
Q

check urine for what 2 things to diagnose DM?

A

ketones and albumin

83
Q

Urine albumin ____ -_____ mg/ 24 hours = Early stage diabetic nephropathy

A

30-299

84
Q

A1C looks back how many days?

A

120

85
Q

Treatment goals for diabetes in non hospitalized patient: A1C, premeal CBG and Postmeal CBG

A

• A1C <7.0
• Premeal CBG 70-130
• Post meal CBG <180
◦ THESE GOALS MAY BE MORE OR LESS STRINGENT DEPENDENT ON PATIENT

86
Q

CBG goals for hospitalized patient

A
  • < 140 mg/dL before meals/ < 180 mg/dL random
  • 140-180 mg/dL for critically ill patients

(higher CBG goal for ill peeps)

87
Q

non surgical interventions for diabetes

A
• CBG monitoring
• Nutrition
• Exercise
• Pharmacotherapies
• Blood glucose monitoring and responding appropriately
• Recognizing signs and symptoms of problems/ complications
• Medication
---> Reduce complications from diabetes
88
Q

surgical interventions for diabetes

A

Pancreas transplant
• Considered “successful” when patient no longer requires insulin and CBG’s are in normal range.
• Complications of transplant rejection and fluid and electrolyte imbalances.

89
Q

Basal insulins and Prandial insulins

A

Basal = Constant amount of insulin
• Intermediate to long acting insulin
• NPH, Lantus, Detemir…

Prandial= Meal-time insulin
• Immediate acting insulin

90
Q

things that affect insulin absorption

A
  • Site: Abdomen is fastest; subq is slower than IM
  • Physical activity- massage, heat, etc increase absorption
  • Timing
  • Type
  • Dose
91
Q

wtf is the dawn phenomenon? + treatment?

A

= Nighttime release of adrenal hormones cause BS to increase around 5-6am.
–>Treatment is to increase insulin at night

92
Q

WTF is Somogyi Phenomenon? + treatment

A

=Hyperglycemia from counter regulation response to nighttime hypoglycemia.
–>Treatment is bedtime snack to prevent hypoglycemia during sleep.

93
Q

• If a patient is NPO, CBG’s are required and _____ insulin will be given. Meal dose insulin will be …..

A

Give basal insulin, withhold meal dose b/c NPO

94
Q

What is our concern with giving IV d50?

A

**hypertonic, caution for extravasation

95
Q

is patient has no IV access but we need to give something to treat hypoglycemia rapidbly what we gonna do?

A

◦ Glucagon IM or Subq, if no IV access.

96
Q

If patient has an acute change in mental status…

A

check CBG!

97
Q

s/s of hypoglycemia

A
  • Sweating
  • Irritability, Anxiety –> Nonresponsive
  • Tremor
  • Tachycardia, Palpitations
  • Hunger
  • Seizure
  • Paralysis
  • AMS
  • Slurred Speech
  • Coma
  • Clumsiness

• Note that patients with Type II DM with chronic hypoglycemia and Type I DM for >30 years may have hypoglycemia unawareness.

98
Q

causes of hypoglycemia?

A
  • Too much insulin/ Inadequate food intake
  • Wrong type of insulin
  • Insulin and meal mismatch
  • Alcohol intake
  • Exercise
  • Kidney failure –> decreased insulin clearance
99
Q

Treatment for hypoglycemia

A
• CHO treatment
• 15-20 g glucose (< 70)
• 30 g glucose (< 50)
• Liquid preferred (Juice, soda)
• Unable to swallow
	◦ SQ/ IM glucagon
	◦ IV D 50 (50% dextrose)
• Repeat blood glucose measurement in 15 minutes, 60 minutes
100
Q

Hyperglycemia s/s

A
Impaired concentration  --> Nonresponsive
• Fatigue
• Warm, Dry  (Hot and dry… sugar high)
• Hunger, Nausea, vomiting
• Headache
• Blurred vision
• Rapid, deep breathing
101
Q

What to do when your patient is NPO ? Hold Insulin?

A
  • Typically don’t hold long-acting insulin

* Typically hold fast acting insulins

102
Q

home glucose meter considerations

A
  • Can use finger or alternate site
  • Warn patients with hypoglycemic unawareness
  • User error is more likely than machine error
  • Infection control
103
Q

Continuous Glucose Monitor considerations

A
  • Intended to supplement capillary readings
  • Sensor, Transmitter & Receiver
  • Provides glucose readings every 1-5 minutes
  • Requires capillary glucose readings for calibration (accuracy)
  • Lag time between capillary glucose and sensor readings (interstitial fluid)
  • Use capillary readings to verify extreme values
104
Q

continuous SQ infusion - what kind of insulin?

A

◦ Basal insulin
◦ Increases at mealtime
◦ Very effective

105
Q

fiber recommendation for diabeted

A

25 G/ day

106
Q

what does alcohol do to CBG?

A

causing a delayed decrease in BG. - limit # of drinks or drink w/ meal

107
Q

exercise and type 1 DM caution

A

don’t exercise if CBG less than 100 or if urine is positive for ketones

108
Q

exercise frequency and type recommendation for DM

A
  • 150 minutes/ week of moderate- intensive exercise OR
  • 75 minutes of vigorous exercise
  • At least 3 days/ week
  • Resistance Exercise at least 2 days/ week
109
Q

exercise consideratinos for diabetes (Safety)

A
  • Avoid extreme temperatures
  • Hydration
  • Wear suitable footwear/ examine feet after exercise
  • Avoid exercise during peak insulin action
  • Eat a CHO snack before
  • Bring candy
  • Check blood glucose throughout day
110
Q

-Diabetics with proliferative or severe retinopathy should avoid

A
  • High intensity CV exercise
  • Resistance weight training
  • Valsava maneuver
111
Q

diabetics who exercise are at risk for

A
  • Retinal detachment
  • Vitreous bleeding
  • Skin Breakdown/ injury
112
Q

skin care for diabetics

A
• Check feet daily for wounds
• Do not walk around barefoot
• Wear appropriate fitting shoes
• Caution with heat or cold
• Avoid personal foot care at home, seek professional assistance (podiatrist)
• Avoid injury from heat sources
• Inspect feet
• Report injuries
• Assess protective sensation
	◦ Semmes-Weinstein monofilaments
113
Q

interventions for visual impairment w/ diabetes

A
  • Coding objects with bright colors (insulin vial)
  • Adjust lighting
  • Large print
  • No pre-filled insulin pens
  • Insulin syringe devices designed for those with visual loss
  • Appropriate selection of glucose monitor
114
Q

Hospital interventions for vision loss diabetes patients

A

◦ Assess and report vision loss
◦ Use vision support when patient is awake
◦ Keep things off the floor
◦ Keep objects within reach