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Endocrine 2 Flashcards

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1
Q

Adrenal cortex “f”

A

in kidneys, secrete steroid hormones

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2
Q

glucocorticoids

A 
affect glucose metab, role in response to stress
inc conversion of protein/fat to glucose
inc breakdown of protein
inc use of fatty acids
dec immune response
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3
Q

mineralocorticoids

A

fluid/elyte balance

aldosterone- Na/H20 retention, K excretion

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4
Q

androgens

A

secondary sex steroids- estrogen/testosterone

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5
Q

Cushings syndrome

A

excess corticosteroids (all 3)

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6
Q

most common cause for cushings synd

A

ACTH secreting pit tumor (cushings disease)

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7
Q

other causes for cushings synd

A

adrenal tumor, ectopic ACTH prod tumor

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8
Q

patho of cushings synd

A

no regulation, inc hormones

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9
Q

CM for cushings synd- gluco

A 
WGPBMED
Wt gain
Glucose intolerance
Protein wasting
Bronze skin
Mood disturbances
Easy bruising, purple striae in abdomen
Delayed wound healing
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10
Q

CM for cushings synd- mineralo

A

H20/Na retention
Wt gain
HTN

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11
Q

CM for cushings synd- androgen

A

acne
men- feminization
women- virilization

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12
Q

DT for cushings synd

A

ACTH inc
serum cortisol inc
urine cortisol inc
BG inc

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13
Q

treatment for cushings synd

A

surgery

meds to suppress cortisol

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14
Q

hyperaldosteronism

A

excess secretion of aldo

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15
Q

patho of hyperaldosteronism

A

excess leads to inc Na and H20 retention=hypervolemia, hypernatremia, excess Ecf
also leads to inc secretion of K=hypokalemia

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16
Q

CM for hyperaldosteronism

A

HTN

hypokalemia

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17
Q

Dt for hyperaldosteronism

A

serum Na inc
serum K dec
serum aldo inc
aldosterone suppression test- give 2 L of IV fluid, see no change

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18
Q

treatment for hyperaldosteronism

A

surgery

meds to control HTN, hypokalemia

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19
Q

addisons disease

A

insufficient “f”

all corticosteroids are dec

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20
Q

etiology of addisons disease

A

autoimmune rxn

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21
Q

patho of addisons disease

A

evel serum ACTH with inadequate corticosteroid synthesis, Adrenal tissue destroyed by ABs against adrenal cortex

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22
Q

CM for addisons disease- gluco

A 
WWND
Wt loss
Weakness/fatigue
N/V
Dec in gluconeogenesis- hypoglycemia
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23
Q

CM for addisons disease- mineralo

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A

KI
K retention
Inc Na/H20 loss

24
Q

CM for addisons disease- androgens

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A

dec axillary/pubic hair

25
DT for addisons disease
``` serum cortisol/aldo dec urine cortisol/aldo dec glucose dec ACTH inc serum k inc ACTH stim tests- see no elev. ```
26
treatment for addisons disease
treat cause replacement steroids diet- inc Na
27
Pancreas "f"
reg BG level insulin- dec BG glucagon- inc BG
28
DM
lack or dec in insulin prod. by B cells of pancreas | or insulin prod is ineffective
29
metab probs for DM
dec utilization of glucose inc fat mobilization inc protein utilization
30
type 1 DM
insulin dependent DM | insulin prod dec or completely absent due to dec in # of b cells in pancreas
31
onset for type 1 DM
less than 40 y.o | rapid progression of symptoms
32
patho of IDDM
genetic factors- HLAs (proteins found on our cells) | autoimmune rxn- viruses
33
type 2 DM
non insulin dependent DM 80% of most cases amt of insulin prod may be normal (inc or dec) but insulin unable to bind with cell receptor sites. Due to defect at receptor sites, dec # of sites or prob with postreceptor sites
34
onset for type 2 DM
older than 40 y.o | slow progression of symptoms, pt able to adjust
35
patho of NIDDM
genetic influence, obesity, age
36
CM for IDDM
3 p's Polyuria Polydipsia Polyphagia
37
CM for NIDDM
``` 3 p's may/may not be present obesity fatigue recurrent inf (UTI) genital pruritis visual change ```
38
DT for DM
random BG level- not always accurate repeated fasting BG oral glucose tolerance test- most accurate
39
treatment for DM
diet- low carb exercise meds
40
meds for IDDM
insulin injections
41
meds for NIDDM
OHAs oral hypoglycemia agents
42
acute complications with DM
DKA- type 1 HHNK- type hypoglycemia
43
DKA
diabetic ketoacidosis glucose accumulates, use fat and protein stores fat->ketones ketones -> metab acidosis and H20 loss protein metabl -> further hyperglycemia hyperglycemia -> osmotic diuresis -> dehydration, hypervolemia, hyperosmolarity. elyte imbalance- K
44
CM of DKA
N/V, hypotension, change in MS, kussmauls resp
45
treatment for DKA
fluid insulin elytes
46
HHNK
hyperosmolor non ketotic coma like DKA but no ketosis. Sever hyperglycemia -> fluid and elyte loss -> hyperosmolarity and hypovolemia
47
CM for HHNK
similar to DKA except no acidosis or ketosis
48
treatment for HHNK
same ask DKA
49
hypoglycemia
BG < 50
50
CM for hypoglycemia
mild: tremors, palpitations, diaphoresis moderate: impaired CNS "f", HA, inability to concentrate, drowsiness severe: disorientation, unconsciousness, seizures, coma
51
treatment for hypoglycemia
quick acting carbs glucagon injection high dextrose (50%) solution IV
52
chronic complications with DM
retinopathy, neuropathy, nephropathy, macrovascular disease, infection
53
retinopathy
deterioration of bld vessels in retina develops rapidly with type 2 scar tissue develops, retina gets detached early CM- blurred vision
54
neuropathy
70% of diabetics, dec in nerve conduction peripheral neuropathy: burning, aching, painful, muscle weakness, sensory loss, loss of fine motor skills, probs with ambulation. potential for injury/undetected injury autonomic nerupathy: affects stomach, bladder GI: gastroparesis- delayed emptying of gastric contents GU: neurogenic bladder
55
macrovascular disease
due to atherosclerosis
56
infection
skin/respiratory

Patho (8 decks)

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