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Patho > Endocrine 2 > Flashcards

Endocrine 2 Flashcards

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

A

KI
K retention
Inc Na/H20 loss

24
Q

CM for addisons disease- androgens

A

dec axillary/pubic hair

25
Q

DT for addisons disease

A 
serum cortisol/aldo dec
urine cortisol/aldo dec
glucose dec
ACTH inc
serum k inc
ACTH stim tests- see no elev.
26
Q

treatment for addisons disease

A

treat cause
replacement steroids
diet- inc Na

27
Q

Pancreas “f”

A

reg BG level
insulin- dec BG
glucagon- inc BG

28
Q

DM

A

lack or dec in insulin prod. by B cells of pancreas

or insulin prod is ineffective

29
Q

metab probs for DM

A

dec utilization of glucose
inc fat mobilization
inc protein utilization

30
Q

type 1 DM

A

insulin dependent DM

insulin prod dec or completely absent due to dec in # of b cells in pancreas

31
Q

onset for type 1 DM

A

less than 40 y.o

rapid progression of symptoms

32
Q

patho of IDDM

A

genetic factors- HLAs (proteins found on our cells)

autoimmune rxn- viruses

33
Q

type 2 DM

A

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
Q

onset for type 2 DM

A

older than 40 y.o

slow progression of symptoms, pt able to adjust

35
Q

patho of NIDDM

A

genetic influence, obesity, age

36
Q

CM for IDDM

A

3 p’s
Polyuria
Polydipsia
Polyphagia

37
Q

CM for NIDDM

A 
3 p's may/may not be present
obesity
fatigue
recurrent inf (UTI)
genital pruritis
visual change
38
Q

DT for DM

A

random BG level- not always accurate
repeated fasting BG
oral glucose tolerance test- most accurate

39
Q

treatment for DM

A

diet- low carb
exercise
meds

40
Q

meds for IDDM

A

insulin injections

41
Q

meds for NIDDM

A

OHAs oral hypoglycemia agents

42
Q

acute complications with DM

A

DKA- type 1
HHNK- type
hypoglycemia

43
Q

DKA

A

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
Q

CM of DKA

A

N/V, hypotension, change in MS, kussmauls resp

45
Q

treatment for DKA

A

fluid
insulin
elytes

46
Q

HHNK

A

hyperosmolor non ketotic coma
like DKA but no ketosis.
Sever hyperglycemia -> fluid and elyte loss -> hyperosmolarity and hypovolemia

47
Q

CM for HHNK

A

similar to DKA except no acidosis or ketosis

48
Q

treatment for HHNK

A

same ask DKA

49
Q

hypoglycemia

A

BG < 50

50
Q

CM for hypoglycemia

A

mild: tremors, palpitations, diaphoresis
moderate: impaired CNS “f”, HA, inability to concentrate, drowsiness
severe: disorientation, unconsciousness, seizures, coma

51
Q

treatment for hypoglycemia

A

quick acting carbs
glucagon injection
high dextrose (50%) solution IV

52
Q

chronic complications with DM

A

retinopathy, neuropathy, nephropathy, macrovascular disease, infection

53
Q

retinopathy

A

deterioration of bld vessels in retina
develops rapidly with type 2
scar tissue develops, retina gets detached
early CM- blurred vision

54
Q

neuropathy

A

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
Q

macrovascular disease

A

due to atherosclerosis

56
Q

infection

A

skin/respiratory

Patho (8 decks)

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