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Endocrine Flashcards

1
Q

when is type I diabetes dx, what happens in type I

A

no insulin production - dx around age 8-13

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2
Q

which diabetes is more common, I or II

A

II

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3
Q

classification of type II diabetes

A

overweight
deficient in insulin and too much glucose (liver)
receptors don’t recognize the insulin
fats are deposited in vascular system for yrs before recognized

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4
Q

what is metabolic syndrome

A

Heart disease, HTN (BP >130/90), High cholesterol, Holding weight in the middle (w>35, m>40), Glucose (101-126)

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5
Q

Classic metabolic syndrome r/t high cholesterol

A

Total Cholesterol>200
LDL>100
Triglycerides >150 (not in good glucose control)
HDL

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6
Q

metabolic syndrome is a high risk for

A

diabetes and cardiovascular disease (sedentary lifestyle)

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7
Q

what ethnic considerations are there for diabetes

A

American Indians

African, Asian, Alaskan Americans

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8
Q

High glucose levels can cause risk for

A

poor wound healing (bacteria loves glucose)
higher risk of dehydration (risk of shock)
electrolyte imbalances (salt goes up, potassium goes down)
cerebral ischemia
osmotic diuresis
decreased erythropoiesis
increased hemolysis
increased risk of thrombosis
impaired gastric motility

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9
Q

preventative measures for cortisol release

A

PPI - prevention of ulcers

Bed rest = risk of clots (lovenox)

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10
Q

when I hold on to salt expect sodium levels to go

A

up

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11
Q

when salt goes up what levels go down

A

potassium

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12
Q

t4 is converted to t3 with

A

iodine

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13
Q

t3 stimulates

A

increases metabolism making things go faster (HR)

helps control warm and hot in the body

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14
Q

some things that put you at risk for hyperglycemia in the hospital setting

A 
pre-existing diabetes
comorbidities (obesity, past med hx of pancreatitis, cirrhosis, hypokalemia)
stress response (cortisol)
aging
lack of muscular activity
insulin deficiency  
dextrose solutions (shakes)
TPN
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15
Q

people w/diabetes are hospitalized more freq, prone to complications, endure longer hospital stays, incur higher costs than pt without diabetes, t or f

A

true

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16
Q

normal A1C level

A

4 - 5.6

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17
Q

an A1C over 7 mean your blood sugar is in this range

A

160-180

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18
Q

how do we dx someone with diabetes

A

fasting blood sugar (NPO 12 hrs) of 126 - more than once

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19
Q

if you eat a fruit eat it with

A

fat and proteins

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20
Q

what is the physiological activity of insulin

A

metabolization of carbs, fats and protein

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21
Q

where is anti-diuretic hormone (adh) stored

A

posterior pituitary

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22
Q

what does adh regulate

A

water balance and serum osmolality

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23
Q

when do we release adh

A 
when osmo receptors notice a change in osmolality
left atrium  (chg in circulating vol. and BP)
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24
Q

osmolality is all about

A

water and particles

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25
Q

when i have a lot of particle and little water it means

A

high particles = high osmolality

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26
Q

adh causes you to

A

hold onto water - causing water RE-ABSORPTION

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27
Q

primary triggers for ADH release (immediate change)

A

increased serum osmolality (high particles, little water)
decreased blood vol.
decreased BP

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28
Q

secondary triggers for ADH release

A 
increased serum sodium levels
trauma
hypoxia
pain
stress 
anxiety
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29
Q

primary cause of diabetes insipidus

A

traumatic injury to posterior pituitary caused by head injury/surgery

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30
Q

can diabetes insipidus be permanent

A

yes - could be autoimmune attacking posterior pituitary

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31
Q

types of DI (diabetes insipidus)

A

neurogenic DI - brain (adh deficiency)

nephrogenic DI - kidney (adh insensitivity)

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32
Q

neurogenic DI means

A

you aren’t producing adh because (brain) is where it lives

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33
Q

nephrogenic DI means

A

producing adh but kidneys are not responding

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34
Q

what can cause neurogenic DI

A

idiopathic
intracranial surgery
infection
severe head trauma

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35
Q

what can cause nephrogenic DI

A

*renal disease
metabolic disturbance
drugs

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36
Q

DI symptoms

A 
polyuria (4-20 L of output)
lots of particles too little water
increased sodium levels
serum osmolality is very high (lots of particles, little water)
urine osmolality is low (lots of pee, no particles)
hypotensive
tachycardia
decreased skin turgor
low RA and PaOP
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37
Q

trt for DI

A

give fluids
adh (vasopressin)
thiazide diuretics (nephrogenic DI) - allows kidneys to recognize adh

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38
Q

what happens in siadh (syndrome of inappropriate anitdiuretic hormone)

A

produce too much adh, hold onto water

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39
Q

***cause of siadh

A

***small cell lung cancer
other neurological issues (stroke, surgery)
TB (not understood why)

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40
Q

what are sodium levels like in siadh

A

really low due to too much water; low particles, high water

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41
Q

what does urine look like w/siadh pt.

A

high osmolality, lots of particle and little water, holding onto urine

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42
Q

s/s of siadh

A 
hypertensive
fluid overload (weak heart=fluid in lungs)
edema
hyponatremia
concentrated urine
decreased BUN, creat, and albumin
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43
Q

when thinking of sodium levels being high or low think

A

change in mental status

44
Q

trt for siadh

A

get rid of fluid - watch i/o carefully

sodium of

45
Q

pheochromocytoma signs and symptoms

A

excess production of epi and nor-epinephrine; severe hypertension

46
Q

dx of pheochromocytoma

A

24 hr urine

47
Q

mgmt of pheochromocytoma

A

remove tumor

1st treatment - alpha blocker 7-10 days before beta blocker to slow HR

48
Q

classic triad for pheochromocytoma

A

severe pounding headache, tachy, profuse sweating

49
Q

characteristics of type I diabetes

A 
toxins/viruses/genetics
abrupt onset
lower prevalence
DKA patients
doesn't have insulin
3 P's
thin
50
Q

what are the 3 P’s of diabetes

A

polyuria
polyphagia
polydipsia
pee, drink, eat ALOT

51
Q

characteristics of type II diabetes

A

obesity/lack of exercise
age >35
slow onset (sore doesn’t heal, freq UTI, chg in vision)

52
Q

the 3 P’s of diabetes is stimulated by

A

high glucose

53
Q

why does pt. with DKA have 3 P’s

A

cells think they need more glucose, doesn’t have insulin
liver produces more glucose causing severe osmotic diuresis
cells are starved so you crave glucose

54
Q

s/s of hypoglycemia

A 
pale and tired
hungry
headache
dizzy
mood swings
blurred vision
palpitations
diaphoretic
slurred speech
nausea
55
Q

s/s of hyperglycemia

A 
freq bed wetting
drowsy
dry mouth
stomach pain
extreme thirst
56
Q

goals for stress induced hyperglycemia

A 
keep glucose between 140-180
insulin protocol (q6hr glucose, cover it dont wait for food)
57
Q

terms for hyperglycemic crises

A

DKA (type I)

HHS (type II)

58
Q

when caring for DKA/HHS

A

check blood sugars freq

adjust insulin dosage freq (pt. specific)

59
Q

if we don’t keep a close eye on glucose levels what can happen with our patient

A

coronary artery disease
retinal disease
ulcers (heels)
surgical wound openings

60
Q

when must a glucose/skin assessment be done

A

within 8 hrs.

61
Q

why do we do a 2am blood sugar

A

somagi effect - sugar drops at 2am, very high in AM

62
Q

rapid acting insulin

A

lispro - epedra

63
Q

if a pt is NPO or on tube feedings what type of insulin should be used

A

regular

64
Q

DKA and HHS are endocrine emergencies, t or f

A

true

65
Q

what happens in DKA and HHS

A

reduction of insulin circulating in body
increase in counter-regulatory mechanisms
glucose is really HIGH
increase in hepatic (liver) glucose production
renal system isn’t getting rid of glucose - sugar is high
unable to use glucose in peripheral tissues

66
Q

long acting insulin

A

lantis

67
Q

factors ldg to DKA/HHS

A 
infection in hospital
omission of diabetic therapy (didn't take insulin)
new onset diabetes (3 p's)
pre-existing/acute illness
stress
68
Q

if a pt is receiving TPN how often should sugar be tested

A

q6hr

69
Q

meds which can cause an increase in blood sugar

A 
steroids
beta blockers (hypoglycemic unawareness)
70
Q

in type I diabetes body is dependent on exogenous insulin, t or f

A

true - even when sick

71
Q

s/s of DKA

A 
severe osmotic diuresis (up to 6L)
extreme dehydration
glucose 500-600 range
increased BUN (breakdown of proteins)
hyperglycemia
hyper/hypokalemia
ketonuria
kussmaul respiration's
increased anion gap
acidosis
metabolism slows
type 1 diabetic 
quick onset
72
Q

pathology of DKA

A

cells without glucose starve - use fat and protein to provide energy for body processes - lead to metabolic acidosis

73
Q

what sign is classic of acidosis

A

kausmal respiration’s (trying to blow off co2)
classic smell - juicy fruit
not a good sign

74
Q

metabolic acidosis leads to a change in

A

anion gap

75
Q

in dka is pt hyper or hypo kalemic

A

can be both

76
Q

electrolytes are badly off while in a hyperglycemic state, t or f

A

true

77
Q

Pt with DKA should be kept on a heart monitor to bring awareness to

A

potassium levels

78
Q

normal anion gap level

A

8-16

79
Q

an elevated anion gap level indicates

A

accumulation of acids

80
Q

we can’t treat potassium or glucose levels in DKA pt until

A

anion gap levels are back to normal

81
Q

DKA or HHS, which has a higher mortality rate

A

HHS

82
Q

s/s of HHS

A 
severe dehydration (up to 9L) - higher mortality
extremely high glucose levels (>1000)
hyperosmolality
older patients
slow to develop
type 2 diabetic
83
Q

difference between HHS and DKA

A

HHS - some insulin is produced - don’t know your sick right away, pt comes in much sicker, more dehydrated

84
Q

pt with HHS is in ketosis, t or f

A

false - no ketosis

85
Q

kausmal respiration’s with DKA equals

A

acidosis

86
Q

mgmt of dka/hhs

A 
respiratory support !
fluid replacement 
insulin drip (dependent on anion gap)
replace electrolytes
check glucose q1hr
87
Q

fluid replacement guidelines for DKA/HHS

A

norm saline - start w/1L bolus
replace 50% of fluid loss in 8 hrs
next 16 hrs remaining fluids

88
Q

insulin pulls what into cells

A

potassium - levels can get low very fast

89
Q

decreased potassium levels are presented by

A

pvc’s on heart monitor

90
Q

should we correct acidosis in DKA pt

A

no, unless pH

91
Q

when pt is receiving insulin drip make NPO, t or f

A

true

92
Q

potassium levels

A

3.5 - 4.5

93
Q

magnesium levels

A

1.5 - 2.5

94
Q

phosphate levels

A

2.4 - 4.1

95
Q

chloride levels

A

96 - 106

96
Q

sick day protocol

A 
never omit insulin - even if not eating normally
sliding scale
q3-4hr glucose checks
q3-4hr ketone checks
take liquid/fluids qhr
97
Q

hypoglycemia is classified as

A
98
Q

what happens during hypoglycemia

A

feel crappy, killing brain cells

99
Q

***1st sign with hypoglycemia

A

chg in mental status, slurred speech

100
Q

what can cause hypoglycemia

A

too much insulin
alcohol
excess exercise

101
Q

s/s of hypoglycemia

A 
tachy
diaphoretic
pale
pupils dilate
SNS preparing for danger
restless
visual disturbances
chg in mental status
difficulty thinking
102
Q

trt for hypoglycemia

A

give this pt glucose - 15 grams of carb orally
50% dextrose
glucagon
oral glucose

103
Q

if pt is unresponsive with hypoglycemia their sugar is

A
104
Q

trt for unresponsive hypoglycemic pt

A

iv access w/D50
1mg glucagon
feed when wakes or asap

105
Q

if a pt tells you they feel low get them an

A

oj

106
Q

what equals 15 grams of glucose

A

3-4 glucose tabs
3-5 hard candies
4oz OJ

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