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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?

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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
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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

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4
Q

T3 aka

A

triiodothyronine

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5
Q

T4 aka

A

thyroxine

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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

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7
Q

goiter is an____
hypertrophy or hyperplasia
hypo or hyperfx

A
  • enlarged thyroid
  • can be hypofx or hyperfx

Could be hypertrophy or hyperplasia

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8
Q

2 types of goiters

A

endemic goiter and toxic goiter

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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)

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10
Q

toxic goiter

A

large nodular gland

d/t hyperactivity

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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

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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

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13
Q

what is exopthalamus

A

eyeballs protruding forward dt fat deposits

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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)

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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
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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

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17
Q

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

A

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

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18
Q

what mainly causes hypothyroidism

A

mainly radiation and surgery for hyperfunction

dec metabolic rate

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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
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20
Q

how is food intake in hypothyroidism

A

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

leads to inc wt

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21
Q

what is the most common hyposecretory state for thyroid

A

Hashimoto’s thyroiditis

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22
Q

Hashimoto’s thyroiditis occurs mostly in

A

90% in middle aged women

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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
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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
Q

Graves disease or hashimotos thyroiditis which involves Tc cells

A

Hashimotos

26
Q

Tx of hypothyroidism

A

if they have an endemic goiter

take T4 daily (lookup why it is??)

27
Q

where are the adrenal glands

how are they divided

what do they produce

A

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
Q

fx of mineralocorticoids, namely aldosterone

A

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
Q

fx of glucocorticoids namely cortisol

A

inc the circulating levels of glucose
suppress the immune sys
potent anti-inflammatory
other effects on metabolism

30
Q

what area of the adrenal gland is most commonly affected

what is this area under the control of

A

the cortex

controlled by pituitary (anterior)

31
Q

Hyperfx (adrenal)

etiology

A

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
Q

are endocrine gland tumors always fx

A

no they can be either fx or nonfx

33
Q

Cushing’s syndrome

A

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
Q

see table 41.4 for Cushing

A

e

35
Q

s

A

d

36
Q

why would someone w Cushing’s get fat deposition to face, neck and abdomen
(buffalo hump and the rounded moon face)

A

cortisol i involved in gluconeogenesis which would cause fat deposition

37
Q

why would someone w Cushing’s get Na and water retention and what could this lead to

A

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
Q

why is a pt w Cushing’s susceptible to infections

A

cortisol is a steroid->anti inflm-> problem w defenses-> susceptible to infection

39
Q

Tx of Cushing’s

A

(this would be to treat tumors or hyperplasia)

  • excise tumor
  • irradiate pituitary (2nd line approach)
  • use drugs for ectopic tumors
  • adrenalectomy
40
Q 
conn syndrome
hypo or hypersec
of which H
un/common
inc in men or women
which gland is affected
A

aldosterone hypersec
uncommon
high in women
adrenal gland

41
Q

etiology of Conn syndrome

A
  • 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
Q

mnfts of Conn syndrome. explanation of them

what is the major problem

A

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
Q

Tx of Conn syndrome

A

-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
Q

when treating an ectopic Cushing’s syndrom tumor what are the 3 categories of drugs/how do they act

A
  1. allow production of the hormone
  2. enzyme inhibitors to suppress synthesis
  3. receptor blockers
45
Q

hypofx disorder of adrenals

A

addison’s disease

46
Q

Addison’s disease

A
  • 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
Q

etiology of Addison’s disease

A

TAIG

tumor,
autoimmunity
infection,
high dose glucocorticoid Tx->dec++ACTH

48
Q

mnfts of Addison’s

A

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
Q

Tx of acute vs chronic Adiison’s disease

A

acute:

  • give IV fluids
  • IV glucocorticoids

Chronic
-glucocorticoids
mineralocorticoids

50
Q

pituitary disorders how is it broken down

A

hyper/hypoactivity

51
Q

which is more affected by disorders anterior or post. pituitary

what are most disorders d/t

A

anterior

mostly d/t adenomas

52
Q

hyperactivity of AP

A

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
Q

SIADH pg 743

A

l

54
Q

ADH is secreted by
fx
acts on

A

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
Q

hyperactivity of PP

A

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
Q

what condition is the opposite of hyperactivity of PP

A

Addison’s

57
Q

How does the RAAS respond to the ++water retention and the dilutional hyponatremia of hyperactivity of PP

A

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
Q

Tx of hyperactivity of PP

A

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)

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