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endo II exam1 > phys II > Flashcards

phys II Flashcards

1
Q

what can cause thyrotoxicosis

A 
graces
factitious thyrotoxicosis
toxic adenoma
toxic nodular goiter
pituitary overproduction of TSH
granulomatous thyroiditis
subacute lymphocytic thyroiditis
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2
Q

What is factitious thyrotoxicosis

A

exogenous thyroid hormone with gland atrophy and low thyroglobulin

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3
Q

what is toxic adenoma

A

hot nodule, over production of thyroid hormone by the nodule with low TSH and gland atrophy surrounding the nodule

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4
Q

what is granulomatous thyroiditis

A

subacute, viral in etiology, with painful gland

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5
Q

what is subacute lymphocytic thyroiditis

A

silent thyroiditis, autoimmune in etiology with non-tender gland, transient
postpartum thyroiditis

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6
Q

what helps to differentiate Dx of causes of thyrotoxicosis

A

radioactive iodine scan

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7
Q

differentiate primary, secondary tertiary hypothyroidism

A

primary is problem in thyroid gland
secondary problem in pituitary
tertiary is problem in hypothalamus

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8
Q

examples primary hypothyroidism

A

hashimotos

T cell mediated

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9
Q

example secondary hypothryoisism

A

pituitary insufficiency

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10
Q

example tertiary hypothyroidism

A

hypothalamic disease

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11
Q

zones of the adrenal gland and what they secrete

A

1) zona glomerulosa- aldosterone
2) zone fasciculata- cortisol and zona reticularis- androgens
3) medulla- epinephrine

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12
Q

what regulates the aldosterone release from adrenal gland

A

Angiotensin II and K

hence why aldosterone leels normal in hypopituitary situation

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13
Q

what controls release of cortisol and androgens in adrenal gland

A

ACTH

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14
Q

what occurs if enzyme 21- alpha hydroxylase is deficient

A

excess adrogens, no glucococorticoids or minerlocorticoids

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15
Q

what occurs is absent 17-alpha hydroxylase

A

increase in mineralocotricoids and absent androgens and low glucocorticoids

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16
Q

what occurs if absent 11 beta hyroxylase

A

absent glucocorticoids and mineralocorticoids, escess androgens

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17
Q

what occurs if absent 17,20 desmolase

A

no androgens

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18
Q

stimualtion for cortisol release

A 
decreased blood cortisol
sleep wake transition
stress, surgery, trauma
pschiatric
ADH
alpha adrengergics,
beta adrengergic antagonists
serotonin
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19
Q

inhibitory factors for cortisol secretion

A

increased blood cortisol
opioids
somatostatin

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20
Q

what negatively feedsback on renin release from kidney

A

decreased Na excretion and H20 excretion and increased K excretion causing increased circulating volume, increase ECvolume, increased BP

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21
Q

what will a decrease in plasma K in kidney cause

A

and increase in K plasma which will stimuate the adrenal Cx

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22
Q

actions of glucocotricoids

A 
increase gluconeogenesis
increase proteolysis
increase liplysis
decrease glucose utilizaiton
decrease insulin sensitivity
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23
Q

actions of mineralocotricoids

A

increase Na resorption
increase K secretion
increase H secretion

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24
Q

actions of adrenal androgens in females

A

stimualte growth of pubic and axillary hair, sitmualte libido

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25
Q

actions of adrenal androgens in males

A

same as testosterone

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26
Q

what is released in times of stress like falling and dislocating hip

A

cortisol, epinephrine and norepi

decrease in the insulin/glucoagon ration

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27
Q

what occurs in a chronically elevated cortisol level patient

A

increase cortisol, increase insulin/glucagon ration
dec epi and norepi
promotes obesity and muscle wasting

28
Q

how does cotisol affect appetite

A

stimualtes appetite and increases insulin/glucagon ration
the high levels cortisol antagonize insulin’s effect on GLUT4 mediated glucose uptake into skeletal muscle and adipose tissue
have glucose intolerance

29
Q

clinical features of addisons

A

hypoglycemia
anorexia, weight loss, nausea, vomiting, weakness, hypotension, hyperkalemia, metabolic acidosis
decreased pubic and axillary hair in females
hyperpigmentation

30
Q

ACTH levels in addisons

A

increased (neg feedback effect of decreased cortisol aka less neg feedback)

31
Q

Tx for addisons

A

replacement glucocorticoids and mineralocorticoids

32
Q

clinical features of cushin syndrome

A

hyperglycemia, muscle wasting, central obesity, round face, supraclavicular fat, buffalo hump, osteoporosis, striae, virilization and menstrual disorders in females, HTN

33
Q

ACTH levels in cushing syndrome

A

decreased (neg feedback from increased cortisol

34
Q

Tx for cushing syndrome

A

ketoconazole

metyrapone

35
Q

ACTH levels in cushing disease

A

increased

36
Q

Tx cushings disease

A

surgical removal ACTH secreting tumor

37
Q

clinical features of Conn syndrome

A

HTN, hypokalemia, metabolic alkalosis, decreased renin levels

38
Q

Tx Conn syndrome

A 
aldosterone antagonists (spironolactone) 
surgery
39
Q

clinical features 21-beta hydroxylase deficiency

A

viralization in females, early acceleration linear growth
early appearance pubic hair
deficient in gluco and mineralocorticoids

40
Q

ACTH levels in 21-B hydroxylase deficiency

A

increased (neg feedback decreased cortisol)

41
Q

Tx 21beta hydroxlyase deficiency

A

replacement of gluco and mineralocorticoids

42
Q

clinical features 17a hydroxylase deficiency

A

lack of pubic and axillary hair in females
Sx for deficient glucocorticoids
Sx excess mineralocorticoids

43
Q

ACTH levels in 17ahydroxylase deficiency

A

increased from decreased cortisol

44
Q

Tx for 17 a hydroxlyase deficiency

A

replacement of glucocorticoids

aldosterone antagonists like spironolactone

45
Q

what is test to Dx cushing

A

overnight DST or late night salivary cortisol or 24 h urine free cortisol

46
Q

if first line of testing + for cushing what is next step

A

confirm positive test with 1-2 additional studies

47
Q

what happens to glucose, aa and fat in fed state

A

insulin increase
there is energy from oxidaiton, synthesis of nitrogens and membranes form aa and fat
storage of glycogen and TAG

48
Q

what occurs in 12 hour fasting

A

TAG broken down to FA–> ketones

gluconeogenesis and glycogenolysis–> glucose

49
Q

GLUT4 R are where

A

skeletal m and adipose tissue

50
Q

where are GLUT2 R

A

liver

51
Q

where are GLUT3 R

A

brain

52
Q

majority of endocrin pancreatic hormones are what

A

insulin then glucagon only 5% is somatostatin

53
Q

action of insulin

A 
increase glucose uptake
increase glycogen fomation
decrease glycogenolysis and gluconeogensis
increase protein syntehsis
increase fat deposition
decrease lipolysis
increas eK uptake
54
Q

effect of insulin on blood level

A

decrease blood glucose, decrease blood aa, FA and ketoacid and blood K

55
Q

stimulatory factors for insulin release

A 
glucose [ [ increase
increase aa, FA and ketoacid
glucagon, cortisol
GIP
K
vagal stimulation, Ach
sulfonylurea drugs
obesity
56
Q

inhibitory factors for insulin secretion

A

decreased blood glucose, fasting, exercise, somatostatin, a-adrenergic agonists, diazoxide

57
Q

effects of insulin on fat

A

increase glucose uptake, increase lipgenesis, decrease liplysis

58
Q

effects of insulin on skel mm

A

increase glucose uptake, glycogen synthesis, protein synthesis

59
Q

effects of insulin on liver

A

dec gluconeogenesis, inc glycogen synthesis, lipogenesis

60
Q

actions of glucagon

A

increase glycogenolysis
increase gluconeogeneis
increase lipolysis
increase ketoacid formation

61
Q

effects of glucagon on blood levels

A

increase glucose, FA and ketoacid in blood

62
Q

stimulatory factors for glucagon release

A

fasting, decreased glucose [ ]
increased aa [ ]
cholecystokinin CCK
beta adrenergic agonists, Ach

63
Q

what are the inhibitory factors for glucagon release

A

insulin, somatostatin, increased FA and ketoacid [ ]

64
Q

what processes are increased with there is a high Insulin:glucagon ration

A

glycogen synthesis, muscle protein synthesis

lipogenesis and TAG formation

65
Q

what processes are increased with a low insulin:glucagon ration

A

glycogen breakdown, gluconeogensis, muscle proteolysis, lipolysis, FA oxidation, ketone body formation

endo II exam1 (14 decks)

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