Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHAR 255 > Thyroid > Flashcards

Thyroid Flashcards

1
Q

What is the thyroid responsible for?

A

Synthesis, storage, and release of T3 and T4

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

What controls the synthesis and release of T3 and T4 ?

A

TSH –> thyroid stimulating hormone

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

what controls TSH?

A

thyrotropin-releasing hormone

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

What is required to create T3 and T4? (3)

A

Iodide, thyroglobulin, and Tyrosine

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

Process of creating T3? T4?

A

Iodide binds to tyrosine attached to thyroglobulin (Mono or diiodotyrosine)
MIT + DIT = T3
DIT + DIT = T4

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

Where is T4 converted to T3?

A

in peripheral tissue (kidney/liver)

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

ratio of T4:T3?

A

13:1

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

Actions of T3 and T4?

A

Heart: chronotropic and inotropic
ADipose tissue: catabolic
Muscle: catabolic
Bone: developmental
Nervous system: developmental
Gut: metabolic
Other: calorigenic

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

what % of T3 in circulation is directly from the thyroid?

A

20%

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

What % of T4 in circulation is directly from the thyroid?

A

100%

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

Which is more potent T3 or T4?

A

T3 ~ 4x more potent

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

what % of T4 is converted to inacive rT3?

A

45%

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

How is thyroid hormone regulated?

A

negative feedback loop

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

what promotes thyroid hormone release?

A

TSH
Low serum iodide

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

What inhibits thyroid hormone release?

A

high T3/T4 levels
Lithium
iodide excess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Male or female more prevalent for thyroid disease?

A

Female; 8/10 pts

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

what % of Canadians have over or under active thyroid glands? how many undiagnosed?

A

10%
>50%

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

What are the 4 common causes of hyperthyroidism?

A

Toxic diffuse goiter (graves disease)
Toxic multi-nodular goiter (plummers disease)
Acute phase thyroiditis
Toxic adenoma

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

Graves disease characteristics?

A

More common in younger, femal pts (20-50yrs old)
most common cause of hyperthyroidism
autoimmune disorder
immune system creates antibodies agaisnt TSH receptors
Can result in hyperplasia of thyroid gland, leading to a goiter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Plummers disease characteristics?

A

Most common in older females (>50)
Most common trigger for nodules to grow is Iodide deficiency
Develops slowly over years

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

Process of development of plummers disease?

A

Iodine deficiency –> less T4 production –> thyroid cells grow larger (multi-nodular goiter) –> TSH receptors mutate –> continually active

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

Acute phase thyroditis characteristics?

A

causes inflammation and damage to thyroid gland
damage = excess hormone release
eventually leads to hypothyroidism once stores are exhausted

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

Toxic adenoma characteristics?

A

benign tumours growing on thyroid gland
tumors become active like thyroid cells and secrete T3/T4 but do not respond to negative feedback loop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Hyperthyroidism non-specific symptoms?

A

Hand tremors
Diarrhea
Heat intolerance
wt loss
weakness
tachycardia
amenorrhea
HTN
anxiety
Afib
increased perspiration
palpitations
soft nails
emotional liabilty
insomnia
hair loss
apathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Graves specific symptoms?

A

exopthalmos (proptosis) –> eye protrusion
Peri-orbital edema –> swelling around eye
diplopia –> double vision
diffuse goiter
pre-tibial myxedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Labs of serum TSH, Free T3, Free T4 in graves?

A

TSH decreased (below 0.1)
T3 increased
T4 normal to increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Labs of serum TSH, Free T3, Free T4 in plummers?

A

TSH decreased (below 0.1)
T3 increased
T4 increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What drug class may increased TSH secretion?

A

1st gen antipsycotics?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Drugs that can increase synthesis and release of T3/T4?

A

Amiodarone
Iodine (chronic use)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What drugs can decrease thyroxin binding globulin?

A

Androgens (likely not clinically significant)
Glucocorticoids (supraphysiological doses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Anti-thyroid drugs?

A

Methimazole
Propylthiouracil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Thioamide MOA?

A

interfere with thyroid peroxidase-mediated processes in T3/T4 production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the thioamides indicated for?

A

Graves
Plummers
pre-treatment before RAI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What does PTU do that MMI does not?

A

inhibits peripheral conversion of T4 to T3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Dosing for MMI?

A

MD: 5-15mg OD for all stages
Intial doses:
Mild = 10-15mg OD
Moderate = 20-30mg OD
Severe = 30-40mg OD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

PTU dosing?

A

Intial dose of 300mg divided BID-TID
MD of 100-150mg divided BID-TID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Thioamides onset? duration of therapy?

A

symptom improvement in 1-4 weeks, thyroid levels should normalize in 2-3months
DoT: 12-18 months common, can tapper down to d/c to see if relapse occurs

38
Q

Common SEs of thioamides?

A

GI upset
rash
arthalgia
abnormal taste/smell
usually go away within 4 weeks

39
Q

Are SEs dose related in thioamides?

A

only for MMI not PTU

40
Q

which thioamide has higher rates of SEs?

A

PTU

41
Q

Serious SEs of thioamides?

A

Neutopenia/ agranulocytosis
hepatotoxicity
Vasculitis

42
Q

What kind of hepatotoxicity is seen with MMI? PTU?

A

MMI –> reversible cholestatic jaundice
PTU –>allergic type hepatocellular damage
both can show increase in AST/ALT, concerned if >3x upper limit or an alcoholic

43
Q

Do you regularly monitor WBCs in thioamide therapy to catch neutropenia/agranulocytosis?

A

No, not cost effective

44
Q

Which thioamide are serious SEs more common in?

A

PTU

45
Q

What can vasculitis lead to?

A

acute renal dysfunction
arthritis
skin ulcers/rashes
respiratory problems

46
Q

What do you tell a patient to watch for when starting thioamide therapy?

A

signs of infection
headache
malaise
sore throat
yellowing of skin (jaundice)
fatigue
weakness
RUQ pain
dark urine

47
Q

DI’s of thioamides?

A

Warfarin (decrease in INR)
Digoxin (increased dig levels)
MMI is a weak Cyp 2D6, 2C9 and 2E1 inhibtor

48
Q

Monitoring of TSH, T3, and T4 for thioamides?

A

TSH T3 and T4
every 4-6 weeks until stable then every 2-3 months for 6-12 months, then 4-6months

49
Q

How to monitor TSH when d/c thioamides?

A

at 3, 6, 12 months then annually

50
Q

when is relapse most common?

A

in first 3 months of d/c

51
Q

What will levels look like if relapse likely?

A

supressed TSH, normal T3/T4

52
Q

What monitoring for thioamides? (not TSH, T3 T4)

A

CBCs, baseline and 1 week after starting
LFTs baseline and 1 week later (watch AST/ALT)

53
Q

Differences between MMT and PTU?

A

MMI quicker onset, less common SEs, better compliance (OD), cheaper, safer in 2nd and 3rd trimester

54
Q

Drug used to control hyperthyroid symptoms?

A

beta-blockers

55
Q

How does radioactive iodine work?

A

taken up by thyroid and causes tissue damage and ablation of gland, defintive treatment compared to thioamides

56
Q

When is radioactive iodine used?

A

mild hyperthyroidism
normal r slightly enlarged gland
no exopthalmous

57
Q

Downside of radioactive iodine?

A

permanent hypothyroidism
can trigger thyroid storm/ thyrotoxicosis
worsen exopthalmous

58
Q

When is radioactive iodine contraindicated?

A

pregnancy and lactation
sever hyperthyroidism
exopthalmous

59
Q

AE’s of radioactive iodine?

A

intial hyperthyroidism exacerbation
followed by hypothyroidism symptoms

60
Q

How is radioactive iodine taken?

A

pre-treatment w/ thioamides 4-6w
stop 3 days prior to RAI stop
restart 3 days after RAI
taper and d/c once thyroid hormone levels decline

61
Q

Patient instructions for RAI?

A

Dont share anything w/ ppl
avoid infants and young children and pregnant women (close contact)
flush toilet 2x after peeing, wash hands well
if neck pain or sore throat develops use acet
if increased nervous, termors, palpitations call doc

62
Q

THyroidectomy for?

A

pregnant who cant tolerate meds
pts who wnat curative but not RAI
pts with large goiters (RAI resistant)

63
Q

Clinical importance of subclinical hyperthyroidism?

A

osteoporosis risk increase
Cardiac abnormalities
Increase in mortality

64
Q

Subclinical hyperthyroidism TSH T3/T4?

A

TSH: 0.1-0.3
free T3/T4 normal

65
Q

Thyroid storm?

A

life threatening condition
severe manifestation of hyperthyroidism
can occur in untreated hyperthyroidism

66
Q

Triggers of thyroid storm?

A

thyroid surgery or RAI
trauma
infection
giving birth

67
Q

What makes thyroid storm life threatening?

A

liver damage
CV collapse
Shock

68
Q

Treatment of thyroid storm?

A

supportive care
corect electrolytes
treat arrythmias
beta blockers to reduce symptoms
anti-thyroid meds
steroids to block T4 –> T3 conversion

69
Q

causes of hypothyroidism? (7)

A

any defect on HPT axis:
1. chronic autoimmune thyroditis (hashimotos)
2. drug induced
3. latrogenic disease (thyroidectomy/RAI)
4. Post-partum thyroiditis
5. chronic iodine deficiency
6. central hypothyroidism
7. hypopituitarism

70
Q

Most common hypothyroid cause?

A

Hashimoto’s disease

71
Q

Characteristics of Hashimoto’s disease?

A

antibodies form and bind to TSH receptors and directly destroy thyroid cells
Other antibodies that interfere w/ T3 and T4 production can form too

72
Q

What drugs can cause hypothyroidism?

A

Lithium: blocks iodine transport into thyroid and prevents hormone release
Amiodarone

73
Q

Clinical presentation of hyothyroidism early disease?

A

wt gain
fatigue
sluggishness
cold intolerance
bradycardia
constipation
heavy menstration
course,dry flakey skin
brittle hair/hari loss
slow and hoarse speech
puffiness around eyes
emotional liability
impaired concentration
+/- non-toxic goiter

74
Q

Clinical presentation of advanced hypothyroidism?

A

Myxedema
hypothermia
confusion
stupor/coma
CO2 retention
hypoglycemia
hyponatremia

75
Q

Lab tests of hypothyroidism?

A

subclinical hypothyroidism:
TSH: increased (4.5-10)
T3/T4: normal
Hashimoto’s:
TSH: very increased (>10)
T3: decreased
T4: decreased (more than T3)

76
Q

Drugs that can decrease TSH?

A

amiodarone, glucocorticoids, metformin

77
Q

Drugs that decrease T4 to T3 conversion?

A

amiodarone
beta blockers
glucocorticoids

78
Q

Drugs that decrease synthesis/release of T3/T4

A

amiodarone
lithium
iodine (acute use)

79
Q

Drugs that increase T3/T4 metabolism?

A

carbamazepine
phenobarbital
phenytoin
rifampin(iftaking levothyroxine)

80
Q

Treatment of hypothyroidism?

A

Desicated thyroid (shit)
liothyronine
levothyroxine
combined T3/T4

81
Q

Why is desicated thyroid shit?

A

causes high peak T3, not well standardized batch to batch

82
Q

Liothyroxine characteristics?

A

Contains T3, no effect on T4
short t1/2
causes wide fluctuations in serum levels
expensive
higher CV effects
dose close to physiological ratio of T4:T3

83
Q

Levothyroxine characteristics?

A

analogue of T4
1st line therapy
t1/2 of 7 days
conversion of T3 regulated by body

84
Q

Levothyroxine dosing?

A

depends on age, wt, cardiac status, severity and duration of hypothyroidism
average replacement dose: 1.6mcg/kg/d
starting dose: 12.5mcg/d to mac wt based
Empirically give 100mcg to healthy pts, 25-50 mcg if subclinical hypothyroidism

85
Q

How to start levothyroxine?

A

start low and titrate up if:
any CVD
rhythm disorders
> 50yrs
Severe, long-standing hypothyroidism
12.5-25mcg and titrate up 12.5-25mcg every 4-6 weeks

86
Q

How must levothyroxine be taken?

A

on empty stomach 30 min before meals or 1 hour after meal, best to take in morning

87
Q

Levothyroxine SEs?

A

hyperthyroid symptoms
cardiac risk increase
aggravate exisitng CVD
BMD reduction

88
Q

Levothyroxine DI’s?

A

absorption reduction: antacids, H2 blockers, PPIs, iron, Ca/mineral supplements, cholestyramine/colestipol
Space these by 2-4hrs
Raloxifene space 12hrs
potent CYP inducers: cipro, phenytoin, carbamazepine, rifampin, pregnancy
TCA’s: increase risk of arrhythmias

89
Q

Levothyroxine monitoring?

A

TSH: aim is low normal values, cant take 4-6 weeks to stabalize with each dosage change
Free T4: normal to slightly elevated
Free T3: normal
Symptoms: improved in 2-3 weeks, maximum effect in 4-6 weeks
once stable/symptom free monitor TSH every 6-12-24m

90
Q

Treat subclinical hypothyroidism?

A

controversial; potentially clincially relevant if;
- atherosclerosis
- HF
- MI
- depression
- low BMD
- metabolic syndrome
Treat if:
- symptoms develop
- pregnancy planning
- HF
- very young pt

91
Q

What to consider if levothyroxine therapy fails?

A

decreased bioavailability:
- poor adherence
- malabsorption
- improper admin
Increased need:
- recent wt gain
- pregnant
- new medicatons taht increased T3/T4 metabolism
Other:
- addisons disease
- alterted HPT axis
- insuffecient peripheral conversion of T4 to T3

PHAR 255 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions