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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
when i have a lot of particle and little water it means
high particles = high osmolality
26
adh causes you to
hold onto water - causing water RE-ABSORPTION
27
primary triggers for ADH release (immediate change)
increased serum osmolality (high particles, little water) decreased blood vol. decreased BP
28
secondary triggers for ADH release
``` increased serum sodium levels trauma hypoxia pain stress anxiety ```
29
primary cause of diabetes insipidus
traumatic injury to posterior pituitary caused by head injury/surgery
30
can diabetes insipidus be permanent
yes - could be autoimmune attacking posterior pituitary
31
types of DI (diabetes insipidus)
neurogenic DI - brain (adh deficiency) | nephrogenic DI - kidney (adh insensitivity)
32
neurogenic DI means
you aren't producing adh because (brain) is where it lives
33
nephrogenic DI means
producing adh but kidneys are not responding
34
what can cause neurogenic DI
idiopathic intracranial surgery infection severe head trauma
35
what can cause nephrogenic DI
*renal disease metabolic disturbance drugs
36
DI symptoms
``` 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 ```
37
trt for DI
give fluids adh (vasopressin) thiazide diuretics (nephrogenic DI) - allows kidneys to recognize adh
38
what happens in siadh (syndrome of inappropriate anitdiuretic hormone)
produce too much adh, hold onto water
39
***cause of siadh
***small cell lung cancer other neurological issues (stroke, surgery) TB (not understood why)
40
what are sodium levels like in siadh
really low due to too much water; low particles, high water
41
what does urine look like w/siadh pt.
high osmolality, lots of particle and little water, holding onto urine
42
s/s of siadh
``` hypertensive fluid overload (weak heart=fluid in lungs) edema hyponatremia concentrated urine decreased BUN, creat, and albumin ```
43
when thinking of sodium levels being high or low think
change in mental status
44
trt for siadh
get rid of fluid - watch i/o carefully | sodium of
45
pheochromocytoma signs and symptoms
excess production of epi and nor-epinephrine; severe hypertension
46
dx of pheochromocytoma
24 hr urine
47
mgmt of pheochromocytoma
remove tumor | 1st treatment - alpha blocker 7-10 days before beta blocker to slow HR
48
classic triad for pheochromocytoma
severe pounding headache, tachy, profuse sweating
49
characteristics of type I diabetes
``` toxins/viruses/genetics abrupt onset lower prevalence DKA patients doesn't have insulin 3 P's thin ```
50
what are the 3 P's of diabetes
polyuria polyphagia polydipsia pee, drink, eat ALOT
51
characteristics of type II diabetes
obesity/lack of exercise age >35 slow onset (sore doesn't heal, freq UTI, chg in vision)
52
the 3 P's of diabetes is stimulated by
high glucose
53
why does pt. with DKA have 3 P's
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
s/s of hypoglycemia
``` pale and tired hungry headache dizzy mood swings blurred vision palpitations diaphoretic slurred speech nausea ```
55
s/s of hyperglycemia
``` freq bed wetting drowsy dry mouth stomach pain extreme thirst ```
56
goals for stress induced hyperglycemia
``` keep glucose between 140-180 insulin protocol (q6hr glucose, cover it dont wait for food) ```
57
terms for hyperglycemic crises
DKA (type I) | HHS (type II)
58
when caring for DKA/HHS
check blood sugars freq | adjust insulin dosage freq (pt. specific)
59
if we don't keep a close eye on glucose levels what can happen with our patient
coronary artery disease retinal disease ulcers (heels) surgical wound openings
60
when must a glucose/skin assessment be done
within 8 hrs.
61
why do we do a 2am blood sugar
somagi effect - sugar drops at 2am, very high in AM
62
rapid acting insulin
lispro - epedra
63
if a pt is NPO or on tube feedings what type of insulin should be used
regular
64
DKA and HHS are endocrine emergencies, t or f
true
65
what happens in DKA and HHS
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
long acting insulin
lantis
67
factors ldg to DKA/HHS
``` infection in hospital omission of diabetic therapy (didn't take insulin) new onset diabetes (3 p's) pre-existing/acute illness stress ```
68
if a pt is receiving TPN how often should sugar be tested
q6hr
69
meds which can cause an increase in blood sugar
``` steroids beta blockers (hypoglycemic unawareness) ```
70
in type I diabetes body is dependent on exogenous insulin, t or f
true - even when sick
71
s/s of DKA
``` 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
pathology of DKA
cells without glucose starve - use fat and protein to provide energy for body processes - lead to metabolic acidosis
73
what sign is classic of acidosis
kausmal respiration's (trying to blow off co2) classic smell - juicy fruit not a good sign
74
metabolic acidosis leads to a change in
anion gap
75
in dka is pt hyper or hypo kalemic
can be both
76
electrolytes are badly off while in a hyperglycemic state, t or f
true
77
Pt with DKA should be kept on a heart monitor to bring awareness to
potassium levels
78
normal anion gap level
8-16
79
an elevated anion gap level indicates
accumulation of acids
80
we can't treat potassium or glucose levels in DKA pt until
anion gap levels are back to normal
81
DKA or HHS, which has a higher mortality rate
HHS
82
s/s of HHS
``` severe dehydration (up to 9L) - higher mortality extremely high glucose levels (>1000) hyperosmolality older patients slow to develop type 2 diabetic ```
83
difference between HHS and DKA
HHS - some insulin is produced - don't know your sick right away, pt comes in much sicker, more dehydrated
84
pt with HHS is in ketosis, t or f
false - no ketosis
85
kausmal respiration's with DKA equals
acidosis
86
mgmt of dka/hhs
``` respiratory support ! fluid replacement insulin drip (dependent on anion gap) replace electrolytes check glucose q1hr ```
87
fluid replacement guidelines for DKA/HHS
norm saline - start w/1L bolus replace 50% of fluid loss in 8 hrs next 16 hrs remaining fluids
88
insulin pulls what into cells
potassium - levels can get low very fast
89
decreased potassium levels are presented by
pvc's on heart monitor
90
should we correct acidosis in DKA pt
no, unless pH
91
when pt is receiving insulin drip make NPO, t or f
true
92
potassium levels
3.5 - 4.5
93
magnesium levels
1.5 - 2.5
94
phosphate levels
2.4 - 4.1
95
chloride levels
96 - 106
96
sick day protocol
``` never omit insulin - even if not eating normally sliding scale q3-4hr glucose checks q3-4hr ketone checks take liquid/fluids qhr ```
97
hypoglycemia is classified as
98
what happens during hypoglycemia
feel crappy, killing brain cells
99
***1st sign with hypoglycemia
chg in mental status, slurred speech
100
what can cause hypoglycemia
too much insulin alcohol excess exercise
101
s/s of hypoglycemia
``` tachy diaphoretic pale pupils dilate SNS preparing for danger restless visual disturbances chg in mental status difficulty thinking ```
102
trt for hypoglycemia
give this pt glucose - 15 grams of carb orally 50% dextrose glucagon oral glucose
103
if pt is unresponsive with hypoglycemia their sugar is
104
trt for unresponsive hypoglycemic pt
iv access w/D50 1mg glucagon feed when wakes or asap
105
if a pt tells you they feel low get them an
oj
106
what equals 15 grams of glucose
3-4 glucose tabs 3-5 hard candies 4oz OJ

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