Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
73 Cards in this Set
- Front
- Back
cells that produce effects growth hormone
a) Kupffer Cells b) Somatotrope Cells c) Pancreatic Cells d) Follicular Cells |
Somatotropes
|
|
T/F
mechanism of GH depends on Somatostatin |
F- somatomedin (produced by LV)
Somatostatin inhibits effects |
|
where is somatomedin produced
a) KD b) LV c) Thyroid d) Pituitary |
LV
|
|
GHRH stimulates GH production and is released from
a) Ant Pituitary b) Post Pituitary c) Hypothal d) None |
Hypothal
GH released from Ant Pit |
|
Incorrect Statement about GH
a) increase rate of protein synth b) uses F.A. as fuel c) lowers blood sugar d) a,b e) b,c |
INCREASES blood sugar bc it decreases use of sugar as fuel
instead GH promotes FA mobilization and use of FA for fuel |
|
GH promotes growth of all of the following except
a) Viceral Organs b) Muscles c) Skin d) Connective Tissue |
promo linear growth of ALL
|
|
when does production of GH Peak?
a) during activity b) after meals c) during sleep d) levels are constant |
during sleep- 3-4 hrs after onset
|
|
stimulates secretion of GH
a) hyperglycemia b) decreased blood AA c) stress d) all |
stress
GH secretion also stim by hypoglycemia/starving increased blood AA |
|
inhibits secretion of GH
a) hyperglycemia b) stress c) increased blood AA d) cortisol |
Hyperglycemia/obesity
Cortisol increased free FA |
|
list causes of short stature
|
genetic
chromosomal chronic illness/malnutrition/malabsorption endocrine psychosocial |
|
T/F
short stature may be idiopathic due to a GH deficiency |
T
also may be due to agenesis/tumor/non working pituitary gland |
|
Congenital GH xu can be determined by
a) amniocentesis b) growth measurement during 1st year c) delayed puberty d) all |
growth measurement during 1st year
obvious by 1st/2nd years |
|
Congenital short stature may cause
a) delayed puberty b) delayed skeletal maturation c) neonate seizure d) all |
ALL
|
|
T/F
tall stature that manifests during childhood is called acromegaly |
F
Gigantism = childhood Acromegaly = adulthood (slow onset) |
|
T/F
a person w acromegaly is more likely to have HPB |
T
due to cardiomegaly also likely to be diabetic- glucose intolerance |
|
HOw will glucose affect lab test results of GH in a px w acromegaly
|
GH will remain Hi and not be suppressed by GH
|
|
which cranial nerve may be compressed in px w acromegaly
a) IV b) II c) III d) V |
II- causes visual field defects
|
|
list manifestation of tall stature disorders
|
glucose intolerance/diabetes
HBP/Cardiomegaly HA Hyperostosis/neuropathy Goiter/heat intolerance CNII compression/visual defect Hypogonadism- low labido, irreg menses |
|
T/F
Acromegaly may cause hypergonadism |
T
Hypogonadism-> lo labido, disturbed menses |
|
Which cell type makes up thyroid hormones
a) Kupffer Cells b) Somatotrope Cells c) Pancreatic Cells d) Follicular Cells |
follicular cells make T3 and T$ from tyrosine and I-
|
|
______is the active form of thyroid hormones
|
T3
|
|
T/F
thyroid hormones do not need to be bound to proteins in the blood |
F
bound to proteins in blood |
|
will signal the hypothal to produce TRH
a) Cold b) Stress c) Sleep d) Heat |
Cold (NOT heat)
Stress Sleep stim hypothal to produce TRH TRH signals Ant Pit to secrete TSH to target thrydoid gland T3/4 travel to target organs/cells |
|
T/F
Thyroid hormones use a + Feedback syst |
F
negative feedback increased production of T3/4 inhibits hypothal from producing TRH which inhibits Ant PIt secretion of TSH |
|
_____ increases metab and protein synth and is necessary for physical and mental development
|
Thyroid Hormone
|
|
Incorrect Statement about Thyroid Hormone
a) vasodilation b) may cause diarrhea c) stimulates parasymp d) catabolism of fat/protein/carbs |
Stimulates SYMPathetic
increases metab and protein synth needed for physical and mental dvlpment. Effects BMR, Cardio/Respiratory sys, GI, and Neuromuscular |
|
Thyroid Hormone increases metab in all tissues except
|
Retina
SP LU Testes |
|
Congenital Hypothyroidism
a) myxedema b) goiter c) grave's disease d) cretenism |
cretenism: infants appear normal- later evident mental retardation and impaired growth
myxedema= adult hypothyroidism -> goiter grave's= hyperthyroidism |
|
cause of transient hypothyroidism
a) Lithium tx b) maternal use of I- c) Hashimoto's d) all |
maternal use of I-
|
|
T/F
Adult hypothyroidism may cause pitting edema |
F
non-pitting myxedema goiter |
|
T/F
Impaired hypothal is the cause of primary hypothyroidism |
F-
primary: thyroidectomy, hashimotos, xs I- ingestion, Lithium tx secondary: caused by impaired hypothal or pituitary |
|
list causes of hyperthyroidism
|
graves disease
adenoma OD thyroid hormone |
|
manifestations of Grave's disease
|
hyperthryoidism/xs symp activity
goiter exophthalmos |
|
mechanism of Grave's Disease
|
autoimmune
abnormal stim of TSH Antibodies act through normal TSH receptors |
|
T/F
Thyroid Storm is likely life threatening |
T
-> hi fever, tachycardia/cardiac failure, agitation, delirium |
|
Conjugation of Adreno-cortical hormones takes place in the
a) LV b) KD c) SP d) GB |
LV- conjugation
excreted via urine and bile |
|
Route of excretion for adreno cortical hormones
a) urine b) feces c) bile d) all |
urine
bile |
|
T/F
Adreno-cortical hormones do not need to be bound to proteins for circulation |
F
must be bound to plasma proteins |
|
not a cause of adrenal insufficiency
a) autoimmunity b) TB c) infection d) xs pituitary function |
xs pituitary function -> cushings
adrenal insufficiency: tumor infection TB autoimmune |
|
pathology of adrenal insufficiency
|
-destruction of all layers of the adrenal gland
-decrease adrenal hormone -increase ACTH |
|
hyper-pigmentation is a manifestation of _______
|
adrenal insufficiency
also: mineral-corticoid xu gluco-corticoid xu |
|
correct statement
a) transient hypothyroidism will cause abnormal brain devlpmnt b) xu of TRH is a disorder of the pituitary c) hashimoto's is the most common cause of primary hypothyroidism d) all are true |
hasimoto's is most common
usually presents in young women |
|
T/F
Graves Disease is an autoimmune condition |
T
-> hypermetabolic state w xs symp activity |
|
T/F
the mechanism of Graves disease causes xs TSH to be released |
F
This is an auto-immune condition: TS-Ab abnormally stim the thyroid gland and act like normal TSH |
|
Px blood test shows lo levels of TSH but px experiences insomnia, hi fever, irritability and constant hunger along w goiter. what is the diagnosis
|
Graves- autoimmune disease TSH-Ab -> xs stim of Thyroid
|
|
list the 3 layers of the adrenal cortex from the outermost layer to the innermost
|
Glomerulosa (aldosterone)
Fasciculata (glucocorticoid) Reticulata (sex hormone) |
|
precursor for steroid hormones
|
cholesterol -> pregnenolone
|
|
list the adrenal cortical steroid hormones produced
|
DHEA
-> testosterone, estradiol/estrone Glucocorticoid Aldosterone |
|
where in the adrenal is Aldosterone synthesized
a) Glomerulosa b) Fasciculata c) Reticulars d) Medulla |
Glomerulosa
|
|
Where is glucocorticoid synth in the adrenal
a) Glomerulosa b) Fasciculata c) Reticulars d) Medulla |
fasciculata
|
|
where are DHEA nad sex hormones synthesized in the adrenal
a) Glomerulosa b) Fasciculata c) Reticulars d) Medulla |
reticularis
(sex hormones released are not as strong as those released from the ovaries/testes |
|
aldosterone is regulated by
a) renin angiotensin b) blood K+ c) ACTH d) FA |
renin angiotensin
blood k+ promo Na/K balance |
|
Where is Na retained by Aldosterone
|
distal tubules
|
|
an xs of blood k+ will cause
a) increase aldosterone for Na+ retention and K+ retention b) decrease aldosterone for Na+ retention and K+ retention c) Increase aldosterone for Na+ retention and K+ excretion d) decrease aldosterone for Na+ retention and K+ excretion |
increase aldosterone for Na+ retention and K+ excretion
|
|
regulation of glucocorticoid occurs by
a) renin angiotensin b) blood K+ c) ACTH d) FA |
ACTH- negative feedback mech of hypothalamic/pituitary adrenal system (peak 6-8 am to deal w stress of waking)
|
|
Glucocorticoid regulation is a ______ feedback system
|
negative
|
|
list the functions of glucocorticoid
|
increase Blood Sugar
Increase protein breakdown -> increase plasma protein increase Fatty Acid mobilization Anti-inflammatory Emotional Stability peaks between 6-8 am |
|
steroid commonly administered in RA treatment
|
glucocorticoid- cortisol
anti-inflammatory action |
|
True Statement about adrenal sex hormone
a) little effect on sexual function b) body hair distribution c) secondary sex characteristics d) all |
All
|
|
adrenal genital syndrome is
a) autosomal dominant b) autosomal recessive c) impaired translocation d) none |
autosomal recessive
-> xu of any one enzyme necessary for the formation of cortisol |
|
describe the mechanism of adrenal genital syndrome
|
Congenital Adrenal Hyperplasia:
xu of any enzyme needed for formation of cortisol -> Increase ACTH -> Adrenal hyperplasia -> Increase Androgen |
|
Manifestation of adrenal genital syndrome
|
baby boy- enlarged genitalia, mineral imbalance
baby girl- virilization syndrome of ambiguous genitalia enlarged clit and fused labia majora (xs testosterone) |
|
Cushing's syndrome
a) adrenal insufficiency b) hypercortisolism c) xs testosterone d) none |
hypercortisolism/xs glucocorticoid
(addison's= adrenal insufficiency) (xs testosteron= drenal genital syndrome) |
|
Causes of adrenal insufficiency
|
Autoimmune
infection TB tumor |
|
adrenal insufficiency affects which layer(s) of the adrenal gland
|
ALL layers destroyed
->decrease in adrenal hormone ->increase ACTH |
|
px presents w fatigue, muscle twitching, mood swings, and dark patches in the gums of the mouth. likley diagnosis
|
adrenal insufficiency/addison's
mnieralcorticoid xu- lo Na+, twitching, fatigue glucocorticoid xu- lo blood sugar, emotions, weightloss hyperpigmentation- esp mucus membranes due to xs ACTH |
|
causes of cushing's syndrome
|
xs pituitary fnctn
adrenal cause ectopic cushing's iatrogenic (xs Rx of steroids- RA, Lupus) |
|
manifestations of cushing's
|
Hyperglycemia
muscle wasting, stretch marks Fat redistribution- moon face, buffalo hump, skinny legs water/electrolyte imbalance- water retention prone to infection Increase ST HCl Euphoria/psychosis Hirsutism, Irreg menses |
|
T/F
extra care should be taking when treating a patient w adrenal insufficiency bc they are more prone to infection |
F
Cushing's more prone to infection -xs steroid production decreases immunity |
|
Px has a puffy round face, skinny legs and hump back. what is the likely diagnosis
|
cushing's
|
|
px diagnosed with cushing's but shows hi levels of plasma ACTH indicates
a) dysfunction of pituitary gland b) dysfunction of adrenal gland c) dysfunction of pineal gland d) none |
dysfunction of post pituitary
|
|
px tests indicate xs excretion of cortisol in the urine and lo plasma levels of ACTH
what does this tell you about the px diagnosis |
cushing's due to dysfunction of adrenal gland
|
|
dexamethasone suppression test is used to diagnose
a) Addison's disease b) Grave's Disease c) Hypothyroidism d) Cushing's disease |
cushing's
if ACTH decreases- the problem is likely to be the adrenal gland if ACTH increase- problem likely to be the pituitary |