phys II Flashcards

(65 cards)

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
actions of adrenal androgens in males
same as testosterone
26
what is released in times of stress like falling and dislocating hip
cortisol, epinephrine and norepi | decrease in the insulin/glucoagon ration
27
what occurs in a chronically elevated cortisol level patient
increase cortisol, increase insulin/glucagon ration dec epi and norepi promotes obesity and muscle wasting
28
how does cotisol affect appetite
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
clinical features of addisons
hypoglycemia anorexia, weight loss, nausea, vomiting, weakness, hypotension, hyperkalemia, metabolic acidosis decreased pubic and axillary hair in females hyperpigmentation
30
ACTH levels in addisons
increased (neg feedback effect of decreased cortisol aka less neg feedback)
31
Tx for addisons
replacement glucocorticoids and mineralocorticoids
32
clinical features of cushin syndrome
hyperglycemia, muscle wasting, central obesity, round face, supraclavicular fat, buffalo hump, osteoporosis, striae, virilization and menstrual disorders in females, HTN
33
ACTH levels in cushing syndrome
decreased (neg feedback from increased cortisol
34
Tx for cushing syndrome
ketoconazole | metyrapone
35
ACTH levels in cushing disease
increased
36
Tx cushings disease
surgical removal ACTH secreting tumor
37
clinical features of Conn syndrome
HTN, hypokalemia, metabolic alkalosis, decreased renin levels
38
Tx Conn syndrome
``` aldosterone antagonists (spironolactone) surgery ```
39
clinical features 21-beta hydroxylase deficiency
viralization in females, early acceleration linear growth early appearance pubic hair deficient in gluco and mineralocorticoids
40
ACTH levels in 21-B hydroxylase deficiency
increased (neg feedback decreased cortisol)
41
Tx 21beta hydroxlyase deficiency
replacement of gluco and mineralocorticoids
42
clinical features 17a hydroxylase deficiency
lack of pubic and axillary hair in females Sx for deficient glucocorticoids Sx excess mineralocorticoids
43
ACTH levels in 17ahydroxylase deficiency
increased from decreased cortisol
44
Tx for 17 a hydroxlyase deficiency
replacement of glucocorticoids | aldosterone antagonists like spironolactone
45
what is test to Dx cushing
overnight DST or late night salivary cortisol or 24 h urine free cortisol
46
if first line of testing + for cushing what is next step
confirm positive test with 1-2 additional studies
47
what happens to glucose, aa and fat in fed state
insulin increase there is energy from oxidaiton, synthesis of nitrogens and membranes form aa and fat storage of glycogen and TAG
48
what occurs in 12 hour fasting
TAG broken down to FA--> ketones | gluconeogenesis and glycogenolysis--> glucose
49
GLUT4 R are where
skeletal m and adipose tissue
50
where are GLUT2 R
liver
51
where are GLUT3 R
brain
52
majority of endocrin pancreatic hormones are what
insulin then glucagon only 5% is somatostatin
53
action of insulin
``` increase glucose uptake increase glycogen fomation decrease glycogenolysis and gluconeogensis increase protein syntehsis increase fat deposition decrease lipolysis increas eK uptake ```
54
effect of insulin on blood level
decrease blood glucose, decrease blood aa, FA and ketoacid and blood K
55
stimulatory factors for insulin release
``` glucose [ [ increase increase aa, FA and ketoacid glucagon, cortisol GIP K vagal stimulation, Ach sulfonylurea drugs obesity ```
56
inhibitory factors for insulin secretion
decreased blood glucose, fasting, exercise, somatostatin, a-adrenergic agonists, diazoxide
57
effects of insulin on fat
increase glucose uptake, increase lipgenesis, decrease liplysis
58
effects of insulin on skel mm
increase glucose uptake, glycogen synthesis, protein synthesis
59
effects of insulin on liver
dec gluconeogenesis, inc glycogen synthesis, lipogenesis
60
actions of glucagon
increase glycogenolysis increase gluconeogeneis increase lipolysis increase ketoacid formation
61
effects of glucagon on blood levels
increase glucose, FA and ketoacid in blood
62
stimulatory factors for glucagon release
fasting, decreased glucose [ ] increased aa [ ] cholecystokinin CCK beta adrenergic agonists, Ach
63
what are the inhibitory factors for glucagon release
insulin, somatostatin, increased FA and ketoacid [ ]
64
what processes are increased with there is a high Insulin:glucagon ration
glycogen synthesis, muscle protein synthesis | lipogenesis and TAG formation
65
what processes are increased with a low insulin:glucagon ration
glycogen breakdown, gluconeogensis, muscle proteolysis, lipolysis, FA oxidation, ketone body formation