Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

old patho 154 > Thyroid problems, pituitary, adrenal > Flashcards

Thyroid problems, pituitary, adrenal Flashcards

1
Q

thyroid location

A

inferior to laryngeal prominence and anterior to…trachea?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

hormones released by thyroid and their functions

where are they made

A 
T4 or thyroxine. and Triiodothyronine T3
-prod in follicular cells of thyroid
-act on nearly every cell in body
function: inc basal metabolic rate, essential to proper development and differentiation. Regulate CHO, protein and fat metb. 
T3 also inc HR and resp rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what stimulates production of T3 and T4

A

Thyrotropin releasing hormone fromt he hypothalamus triggers the release of TSH from the anterior pituitary. TSH stim the release of t3 and t4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

T3 aka

A

triiodothyronine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

T4 aka

A

thyroxine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

diff between T3 and T4

A

T4 is at 20x conc to T3. T3 is the active form of T4. T4 gets converted to T3 in the cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

goiter is an____
hypertrophy or hyperplasia
hypo or hyperfx

A
  • enlarged thyroid
  • can be hypofx or hyperfx

Could be hypertrophy or hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

2 types of goiters

A

endemic goiter and toxic goiter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

endemic goiter

A

-iodine def-> dec T3 and T4-> compensatory inc in TSH-> hyperplasia and hypertrophy

iodine is nec to synthesize T3 and T4. (without idodine you can form T3 and T4 but they arent fx. this occurs most in places w dietary def)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

toxic goiter

A

large nodular gland

d/t hyperactivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

hyperthyroidism is mostly d/t _____

does the outcome make sense\?

A

autoimmunity

this is counterintuitive as you would expect it to cause hypothyroidism. In this case an Ab binds to thyroid receptor and acts as TSH and inc T3 and T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Graves disease
uncommon?
affects
3 hallmarks

A

is the most common form (80-90%) of hyperthyroidism
-autoimmunity affcts young women most

3 hallmarks
1=goiter
2=hyperthyroidism
3=exopthalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is exopthalamus

A

eyeballs protruding forward dt fat deposits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

patho of Grave’s disease

A

TSAbs mimic the action of TSH

  • autoimmunity targets TSH receptors on thyroid cells
  • TsAbs (TSI) mimic TSH an bind to TSH receptors-> TH secretion
  • inc TH inhibits TSH secretion
  • dec TSH
  • TSAbs avoid enzyme degradation and are active longer

theres no T cell involvement

involves Thyroid stimulating Abs which mimic the action of TSH (it doesnt involve T cells)
(-the TSAbs replace TSH on thyroid cell which inc T3 and T4 levles which through negative feedback inhibits TSH release.)
(normally when TSH has bound to receptors this complex is broken down by enzymes but not for TSAbs which leads to enlargement of gland d/t TSAbs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is thyrotoxicosis

patho/what results

A

-clinical presentation of (Grave’s disease) hyperthyroidism

  • inc metb results (altered metb pathways)
    • inc protein and lipid metb (wt loss) when metabolizing heat is a product. 70% of heart is to warm the body the other 30% is for ATP. you now have excess heat
    • metb heat->compromized heat loss mechanisms-> flushed skin and perspiration
    • intolerance to inc Temp
    • inc HR and inc Co to meet inc demand for 02 and waste removal
    • a byproduct of all of the metb is C02 in order to remove it they will be hyperventilating
    • excitable, irritable, insomnia, anxiety
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Tx for Grave’s disease

A

1 of 3 options
- antithyroid drugs (eg tapazole) which suppresses prod of T3 and T4
-radioiodine therapy (binds to thyroid selectivley and local radiation detroys
Sx for large goiters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

hypothyroidism. where can the problem be? which is most common

A

primary thyroid, (95%)
secondary pituitary,
tertiary hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what mainly causes hypothyroidism

A

mainly radiation and surgery for hyperfunction

dec metabolic rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

problems of hypothyroidism

A
  • dec body T
  • dec Co d/t def of energy
  • very dec CNS fx
  • weak muscle action (d/t dec ATP)
  • inc wt
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

how is food intake in hypothyroidism

A

food intake will be normal but unable to metb->inc storage

leads to inc wt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the most common hyposecretory state for thyroid

A

Hashimoto’s thyroiditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Hashimoto’s thyroiditis occurs mostly in

A

90% in middle aged women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

hashimotos thyroiditis

A

most common hypothyroidism

  • 90% occurs in middle age women
  • autoimmune destr of gland
  • antithyroid Abs block TSH binding
  • lymphocyte infiltrates (there is some degree of classic autoimmunity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

how does the autoimmune destr of Hashimotos thyroiditis take place

A

The abs bind to TSH receptors and block the receptor which doesnt allow TSH to bind-> atrophy

25
Graves disease or hashimotos thyroiditis which involves Tc cells
Hashimotos
26
Tx of hypothyroidism
if they have an endemic goiter | take T4 daily (lookup why it is??)
27
where are the adrenal glands how are they divided what do they produce
there are two. they lie superior to the kidneys and inferior to the diaphragm. They are retroperitoneal divided into the adrneal cortex (on the outside) produces: mineralocorticoids (aldosterone) glucocorticoids (cortisol) androgens (male sex hormones) (in the male body this has little effect as the testes produce androgens) the medulla which produces NE and E (catecholamines)
28
fx of mineralocorticoids, namely aldosterone
minerocorticoids reguate sodium (mineral) In kidneys, aldosterone acts on DCT and CD by inc the reabsorption of sodium and the excretion of both potassium and hydrogen ions
29
fx of glucocorticoids namely cortisol
inc the circulating levels of glucose suppress the immune sys potent anti-inflammatory other effects on metabolism
30
what area of the adrenal gland is most commonly affected what is this area under the control of
the cortex controlled by pituitary (anterior)
31
Hyperfx (adrenal) | etiology
cortical tumor or hyperplasia-> inc++cortisol, dec adrenocorticotropic hormone - tumor or hyperplasia of anterior pituitary->inc++ACTH - ectopic ACTH sec tumour (eg in lung)
32
are endocrine gland tumors always fx
no they can be either fx or nonfx
33
Cushing's syndrome
glucorticoid hypersecretion-> inc++ hormone action -protein catabolism (weak muscles) and fat deposition in face, neck, abd gluconeogenesis prolonged hyperglycemia - I resistance - IGT Na and water retention (HTN and hypokalemia) it shouldnt have rounded moon face susceptible to infections androgen hypersec?? buffalo hump
34
see table 41.4 for Cushing
e
35
s
d
36
why would someone w Cushing's get fat deposition to face, neck and abdomen (buffalo hump and the rounded moon face)
cortisol i involved in gluconeogenesis which would cause fat deposition
37
why would someone w Cushing's get Na and water retention and what could this lead to
cortisol in normal levels doenst have fx r/t fluid balance but in excess it does have minero fx and can act like aldosterone. could lead to HTN and hypokalemia
38
why is a pt w Cushing's susceptible to infections
cortisol is a steroid->anti inflm-> problem w defenses-> susceptible to infection
39
Tx of Cushing's
(this would be to treat tumors or hyperplasia) - excise tumor - irradiate pituitary (2nd line approach) - use drugs for ectopic tumors - adrenalectomy
40
``` conn syndrome hypo or hypersec of which H un/common inc in men or women which gland is affected ```
aldosterone hypersec uncommon high in women adrenal gland
41
etiology of Conn syndrome
- usually cortical adenoma - idiopathic cortical hyperplasia - renin secreting renal tumor WHY? RAAS stim the prod of aldosterone by AII. also stim ADH. Renin will stim inc aldosterone
42
mnfts of Conn syndrome. explanation of them what is the major problem
major problem: HTN (d/t aldosterone inserting sodium channels-> Na retention and water will follow-> hypervolemia->HTN) -hypokalemia and alkalosis WHY? (aldosterone excretes K and Hydrogen which inc pH)
43
Tx of Conn syndrome
-adrenalectomy for adenoma (unilateral) (w hyperplasia you dont excise, you either suppress H or allow H prod and use receptor blocker) drugs for hyperplasia aldosterone receptor antagonist na restriction
44
when treating an ectopic Cushing's syndrom tumor what are the 3 categories of drugs/how do they act
1. allow production of the hormone 2. enzyme inhibitors to suppress synthesis 3. receptor blockers
45
hypofx disorder of adrenals
addison's disease
46
Addison's disease
- primary def of the cortex of adrenal gland. - all 3 groups of hormones are affected (Making up for the def is diff because it secretes 3 H) uncommon
47
etiology of Addison's disease
TAIG tumor, autoimmunity infection, high dose glucocorticoid Tx->dec++ACTH
48
mnfts of Addison's
fluid losses (Na, Cl)-> hypovolemia-> dec CO-. HoTn-> weakness, fatigue -dec GAS? gastric acid sec? wt loss WHY? LOOKUP! 1. if not taking meds. 2. if taking meds and facing stress theyll go into Addisonian crisis: acute insuff d/t stress (can be fatal
49
Tx of acute vs chronic Adiison's disease
acute: - give IV fluids - IV glucocorticoids Chronic -glucocorticoids mineralocorticoids
50
pituitary disorders how is it broken down
hyper/hypoactivity
51
which is more affected by disorders anterior or post. pituitary what are most disorders d/t
anterior mostly d/t adenomas
52
hyperactivity of AP
adenomas (trophic and non trophic Hormones). (if its a trophic hormone youll see impact on target gland if its non-trophic problem will be in body on target cells. hyperactivity of target gland
53
SIADH pg 743
l
54
ADH is secreted by fx acts on
secreted by PP but made in hypothalamus fx: increases water permeability of the CD and DCT by inducing translocation of aquaporin-CD water channels in the plasma membrane of collecting duct cells also sodium reabsorption
55
hyperactivity of PP
syndrome of inappropriate ADH (SIADH) - hypersec of ADH - ectopic tumor secretes ADH-like substance eg in lungs - ADH prevents water loss, Na follows-> fluid retention - dilutional hyponatremia
56
what condition is the opposite of hyperactivity of PP
Addison's
57
How does the RAAS respond to the ++water retention and the dilutional hyponatremia of hyperactivity of PP
RAAS is triggered by dec renal perfusion but the pt has hypervolemia so no renin is released. The RAA would cause an inc in aldosterone but since this does not happen sodium is not retained
58
Tx of hyperactivity of PP
diuretic (coud cause them to lose more sodium) -restrict fluid intake if mild to address cause: ADH antagonists (aquaretics block ADH receptor

old patho 154 (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions