Endocrine 2 Flashcards
Adrenal cortex “f”
in kidneys, secrete steroid hormones
glucocorticoids
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
mineralocorticoids
fluid/elyte balance
aldosterone- Na/H20 retention, K excretion
androgens
secondary sex steroids- estrogen/testosterone
Cushings syndrome
excess corticosteroids (all 3)
most common cause for cushings synd
ACTH secreting pit tumor (cushings disease)
other causes for cushings synd
adrenal tumor, ectopic ACTH prod tumor
patho of cushings synd
no regulation, inc hormones
CM for cushings synd- gluco
WGPBMED Wt gain Glucose intolerance Protein wasting Bronze skin Mood disturbances Easy bruising, purple striae in abdomen Delayed wound healing
CM for cushings synd- mineralo
H20/Na retention
Wt gain
HTN
CM for cushings synd- androgen
acne
men- feminization
women- virilization
DT for cushings synd
ACTH inc
serum cortisol inc
urine cortisol inc
BG inc
treatment for cushings synd
surgery
meds to suppress cortisol
hyperaldosteronism
excess secretion of aldo
patho of hyperaldosteronism
excess leads to inc Na and H20 retention=hypervolemia, hypernatremia, excess Ecf
also leads to inc secretion of K=hypokalemia
CM for hyperaldosteronism
HTN
hypokalemia
Dt for hyperaldosteronism
serum Na inc
serum K dec
serum aldo inc
aldosterone suppression test- give 2 L of IV fluid, see no change
treatment for hyperaldosteronism
surgery
meds to control HTN, hypokalemia
addisons disease
insufficient “f”
all corticosteroids are dec
etiology of addisons disease
autoimmune rxn
patho of addisons disease
evel serum ACTH with inadequate corticosteroid synthesis, Adrenal tissue destroyed by ABs against adrenal cortex
CM for addisons disease- gluco
WWND Wt loss Weakness/fatigue N/V Dec in gluconeogenesis- hypoglycemia
CM for addisons disease- mineralo
KI
K retention
Inc Na/H20 loss
CM for addisons disease- androgens
dec axillary/pubic hair
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.
treatment for addisons disease
treat cause
replacement steroids
diet- inc Na
Pancreas “f”
reg BG level
insulin- dec BG
glucagon- inc BG
DM
lack or dec in insulin prod. by B cells of pancreas
or insulin prod is ineffective
metab probs for DM
dec utilization of glucose
inc fat mobilization
inc protein utilization
type 1 DM
insulin dependent DM
insulin prod dec or completely absent due to dec in # of b cells in pancreas
onset for type 1 DM
less than 40 y.o
rapid progression of symptoms
patho of IDDM
genetic factors- HLAs (proteins found on our cells)
autoimmune rxn- viruses
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
onset for type 2 DM
older than 40 y.o
slow progression of symptoms, pt able to adjust
patho of NIDDM
genetic influence, obesity, age
CM for IDDM
3 p’s
Polyuria
Polydipsia
Polyphagia
CM for NIDDM
3 p's may/may not be present obesity fatigue recurrent inf (UTI) genital pruritis visual change
DT for DM
random BG level- not always accurate
repeated fasting BG
oral glucose tolerance test- most accurate
treatment for DM
diet- low carb
exercise
meds
meds for IDDM
insulin injections
meds for NIDDM
OHAs oral hypoglycemia agents
acute complications with DM
DKA- type 1
HHNK- type
hypoglycemia
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
CM of DKA
N/V, hypotension, change in MS, kussmauls resp
treatment for DKA
fluid
insulin
elytes
HHNK
hyperosmolor non ketotic coma
like DKA but no ketosis.
Sever hyperglycemia -> fluid and elyte loss -> hyperosmolarity and hypovolemia
CM for HHNK
similar to DKA except no acidosis or ketosis
treatment for HHNK
same ask DKA
hypoglycemia
BG < 50
CM for hypoglycemia
mild: tremors, palpitations, diaphoresis
moderate: impaired CNS “f”, HA, inability to concentrate, drowsiness
severe: disorientation, unconsciousness, seizures, coma
treatment for hypoglycemia
quick acting carbs
glucagon injection
high dextrose (50%) solution IV
chronic complications with DM
retinopathy, neuropathy, nephropathy, macrovascular disease, infection
retinopathy
deterioration of bld vessels in retina
develops rapidly with type 2
scar tissue develops, retina gets detached
early CM- blurred vision
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
macrovascular disease
due to atherosclerosis
infection
skin/respiratory
