Path Spring 15 Thyroid

Front 1

c cells in the thyroid secrete what, what does that substance do

Back 1

calcitonin- lowers serum Ca

Front 2

whats TPO

Back 2

thyoid peroxidase- it oxideses iodine so it can be used to make T3/4

Front 3

what is the TSH in...

1. primary hyperthyroidism
2. primary hypothyroidism

Back 3

1. hyper- low
2. hypo- high

euthyroid is when its in range

**TSH is the best test to dx thyroid problems, can confirm with a T4

Front 4

if THS is....

1. low
2. high

what do you expect, adn whats the next test

Back 4

1. TSH LOW, think hyperthyroid, get T4 to confirm. if for some reason its low it can be T3 toxicosis or subclinical hyperthyroid

2. TSH HIGH, think hypothyroid, get T4 and anti TPO. If T4 is low and TPO is + its hashimoto

Front 5

This 73 y/o female c/o nervousness and weight loss. She first noticed symptoms following a car accident 2 months previously in which she suffered minor injuries. She first attributed the
symptoms to anxiety about the accident but sought medical advice after a 15 pound weight loss.
• Past history significant for CHF, COPD
Physical exam reveals a thin, nervous‐appearing
woman. BP 180/62, pulse 112, weight 138 pounds,
height 64 inches. There is no exophthalmos. The
thyroid is palpably diffusely enlarged.
 Lab: TSH, sensitive, 0.03 mIU/ml (0.3‐5.0) T4 (free) 11.2 ug/dL (1.2‐4)
• This patient is: a) Euthyroid,
b) Hyperthyroid,
c) Hypothyroid
• What are the possible causes of her condition?

Back 5

hyperthyroid

cause of hyperthyroid: can have AB stim TSH receptors

Front 6

thyrotoxicosis

Back 6

hypermetabolic state bc of high T3/T4

Front 7

whats hyperthyroidism, whats the most common cause

Back 7

thyrotoxicosis bc thyrodi makes too much T3/4

Front 8

what are cases of thyrotoxicosis NOT due to hhyperthyroidism

Back 8

the thyroid"ITIS"

Front 9

A 42 y/o woman with a history of pernicious
anemia comes to the physician c/o increased
anxiety, heart palpitations, heat intolerance,
unexplained weight loss, and multiple daily
bowel movements. She has not had a period
in 4 months. On PE, the patient is found to
have a goiter, a thyroid bruit, and mild
proptosis
Labs: free T4 increased; triiodothyronine inc.;
TSH undectectable.
42 y/o woman. What is the most likely
etiology of this patient’s disease?
A) Autoimmune stimulation of TSH receptors
B) Idiopathic replacement of thyroid by
fibrous tissue
C) Thyroid adenoma
D) Thyroid hormone‐producing ovarian teratoma
E) Viral infection leading to destruction of
thyroid tissue

Back 9

hyperthyroid- graves

**the pernicious anemia is AI, AI disease often goes together

**AI stimulation of TSH receptors

Front 10

clinical manifestations of thyrotixicosis *hyperthyroid)

Back 10

1. increased metabolism
2. increased SNS

1. heat intolerance
2. lots of stool
3. tachy, wide PP, palpitations, a fib, cardiomyopathy ***FIRST
4. anxious
5. big old eyes
6. sweaty, warm, flushed
7. infiltrating dermopathy (pretibial myxedema) shin skin is orange peel like
5.

Front 11

if your pt has thick ankle skin, is it hyper or hypothyroid

Back 11

hyer

**there are Thyroid receptors on the skin so it thickens with all the excess input

Front 12

hyperphagia and weight loss

Back 12

hyperthrooid- graves- goiter

Front 13

hyperthyroid effects on skeletal system

Back 13

increased turnover, osteoperosis,

alk phos is high

Front 14

what happens in a thyroid storm

Back 14

1. abrupt hyperthyroidism
2. graves
3. due to increase catecholamines- febrile, tachy,
4. can be an arrhythemia- EMERGENCY, tx w/b blocker

Front 15

what are the labs in graves

what lab is specific to graves

Back 15

its hyperthyroid so...

TSH low
T3/4 High
RAI high- large gland
ALK phos HIGH

Front 16

whats the triad of graves

Back 16

1. hyperthyroid- goiter
2. exopthalmous- infiltrative opthalomapathy (TSH R on eye mm)
3. pertibial myxedema

Front 17

whats graves associated with

Back 17

other AI

addisons-
vitiligo
SLE
Downs

Front 18

what disease uses AB to mimic TSH

whats the tx

Back 18

graves- hyperthyroidism

tx with thyroid blockers- PTU, methimazole, b blockers to stop SNS effects

Front 19

This 17 y/o girl presented with 1 mon. history
of weight loss, increased appetite, mild
insomnia, hand tremor, palpitations,
sweating, heat intolerance, and quick loss of
temper. Daily bowel movements had
increased from 1 to 2. There is no family
history of thyroid disorders.
• PE: Blood pressure 120/80, p104, lid lag and
mild exophthalmus, thyroid 2.5 x normal
size with bruit heard over thyroid.

what are the sig points in hx

what is the disease

what are the labs

Back 19

weight loss, eat more, tremor, palpitations, sweat, heat intolerance, BM increase.

graves- hyperthyroid

TSH low
T3/4 high
TPO AB -

common in asian, kids are tall

Front 20

what are the causes of hypothyroidism

Back 20

1. not enough tissue- abnormal location,
surgery, radation
2. goitrous- not enough hornome production
3. AI- hashimoto, most common
4. drugs
5.I deficit

Front 21

whats the lab for hypothyroidism

Back 21

TSH increased
T3/4 decreased
increased creatine kinase
increased cholesterol

Front 22

A 7 y/o girl is brought to the ED by her
parents because of concerns that she is not
growing and not developing appropriately. The
parents say that the patient has cold intolerance
easy fatigability, and polyuria. PE is notable for
short stature and bilateral papilledema. TSH and
free T4 are low. MRI shows a multilobated
suprasellar mass with ring calcification in the
region of the sella turcica.

the lesion visualized on MRI represents a
primary intracranial neoplasm, what is the most
likely diagnosis?
A) Craniopharyngioma
B) Ependymoma
C) Hemangioblastoma
D) Prolactinoma
E) Thyrotropinoma

Back 22

craniophayyngioma

cold, fatigue, polyuria

Front 23

sheehan syndrome

Back 23

pit necrosis from birth

**can cause 2 hypothyroidism

Front 24

Baby girl “B” is a monozygotic twin, born at
37 wks. gestation. Newborn physical exam
was normal. Neonatal testing for genetic dis.
and thyroid function in hospital was “normal”
• Twins were similar in weight and development
at 6 wk. checkup.
• Seen at 8 mon., twin B was the “good” baby
who slept all night and rarely cried. Twin B, unlike her sister, had not tried to
sit up. She appeared pale. Physician
reassured parents that she was normal.
• At 10 mon. , mother requested a complete
physical due to failure to grow.
• Twin B was referred to a pediatrician who
interpreted infants physical finding as due
to “poor feeding” and iron deficiency anemia
‐ Hb 8.8 gm (normal 11) .

Iron was prescribed. CBC was repeated
and demonstrated little change. Iron
injections were given to age 14 mon.
The anemia persisted but parents were
reassured that the anemia would eventually
correct with continued therapy.
• At 16 mon. parents sought consultation with
another pediatrician. Thyroid function tests
were performed that demonstrated elevated
TSH and low free T4.

Back 24

hypothyroid!!! law suite

congenital hypothyroid is creatinism

Front 25

whats creatinism

causes?

Back 25

hypothyroid in a baby

caused: I deficient, enzyme deficit, poor thyroid development

*mom can give thyroid via placenta

Front 26

what are hte features of fetal/infant hypothyroid. what is this condition called

Back 26

cretinism- poor development, no I, no enzyme

Clinical: FLOPPY baby, retarded, short, skeletal problems, coarse face, protruding tongue, umbilical hernia

Front 27

A 4 y/o child whose family arrived in the US
from Ecuador last month is brought to the
pediatrician for a checkup. On PE, the patient
is found to be short, pot‐bellied, and pale with
a puffy face, a protruding umbilicus, and
a protuberant tongue. The child shows clear
signs of significant mental retardation. Which
of the following labs should be ordered and
what results are expected?

Back 27

cretin- hypothyroid

TSH high
T3/4 low
creatine kinase high
cholesterol high

Front 28

A 23 y/o female has a 2 yr. history of cold
intolerance, , fatigue and amenorrhea. She has
gained over 200# in 8 years. Her family reports
that her speech is extremely slow and coarse.
Family history is remarkable for obesity‐mother
weighs over 600#.
• Physical exam: morbidly obese female 420#, BP
122/70, pulse 50. She has puffy facies, 2+ pedal
edema. Muscle stretch reflexes are markedly
prolonged in relaxation phase

She speaks in a deep, coarse, “gravelly” voice
with extremely slow phonation.
1. She is probably:
 a) euthyroid
 b) hyperthyroid
 c) hypothyroid
2. On what do you base your diagnosis?
3. What lab tests should be performed

Back 28

1. hypothyroid= myxodema

1. cold intolerance, speech is slow and corarse, weigh gain, no period,

3. what labs do you do:
TSH high
T34 low
creatine kinase high

Front 29

whats myxedema-

Back 29

hypothyroid

seen in adults (CRETINISM WAS kids)
insidious onset, fatigue, apathy,
mental slowness
menorrhagia
constipation
SOB
cold intolerance (skin is pale and cold in hypo. in hyper it was warm and moist)

Front 30

your pt has puffy face, dry skin, coarse hair, scant pubic hair, thin eyebrowa, is htis hyper or hypo thyrodi,

Back 30

hypo, myxedema

tongue gets biiig

Front 31

This 47 y/o woman has had constipation,
weakness, fatigue and dry skin for 2 mon.
During this time she has experienced moderate
weight gain and menorrhagia.
• On physical exam, there is thinning of scalp
hair, coarse skin and bilateral leg swelling.
Bradycardia and delayed relaxation of the
deep tendon reflexes of the arms are present.
• Thyroid is symmetrically enlarged, nontender

Back 31

myxedema, hypothyroid

tounge gets mig

Front 32

serum cholesterol and CK are elevated in what....

Back 32

hypothyroidm (myxedema)

Front 33

why do ppl with myxedema get fat?

is hypothyroidism a likely cause of obesity

Back 33

mucopolysaccharide buid up

seen in sub cu
vocal cords
tongue

**not likely to cause obesity bc you have DECREASED appetite

Front 34

whats the dif btwn myxedema and hashimoto

Back 34

both are HYPOthyroid

myxedema is caused by low production
hashimoto- AI destruction, chonic lymphocytic thyroiditis

Front 35

hashimoto

1. pathogenesisi
2. labs
3. micro

Back 35

1. AI destruction, genetic destruction HLA DR5. CD8 mediated death, cytokine death, AB dependent death --> dead thyrocytes


2. LABS
TSH high
T3/4 low
Thyroglobulin AB present
Anti TPO AB present

3. lymphocyte infiltrate
2.

Front 36

hashimoto is common in what

Back 36

turner
downs
vitelligo
SLE
ra

other AI diseases

Front 37

what does the immune system do to kill the thyroid in hashimoto

Back 37

1. CTL
2. AB
3. cytokine,

employs all 3 death mechs

Front 38

what are pts with hashimoto at risk for

Back 38

B cell MALT

Front 39

in hashimoto waht happens to thyroid fx

Back 39

transient increase bc os the cells are killed they release hormone, then its HYPOthyroid

Front 40

what does the thyroid look like in hashimoto

Back 40

moderate enlarge
rubber, nodular, fleshy cut surface

**this is a MUST KNOW pic
*then micro is all lymphocytes, this is why they get B cell MALT

Front 41

A 38 y/o attorney reported at her annual
physical exam p y that she was tired, had difficulty
concentrating on her work and a noticeable
decline in her memory over the past several
months. She attributed these symptoms to stress
due to her legal case load.
• She admitted that her frequency of bowel
movements had decreased from once daily 6
months ago to once every 2‐3 days. She was
having difficulty avoiding weight gain. Despite warm weather, she felt chilled w/o a
sweater. Her only medication was an oral
contraceptive.
• PE revealed a well‐proportioned woman, 65
inches tall, 124 lb with sparse eyebrows at lateral
margins. There was a diffusely moderately
enlarged thyroid gland on palpation. Despite warm weather, she felt chilled w/o a
sweater. Her only medication was an oral
contraceptive.
• PE revealed a well‐proportioned woman, 65
inches tall, 124 lb with sparse eyebrows at lateral
margins. There was a diffusely moderately
enlarged thyroid gland on palpation

Back 41

hypothyroid- hashimoto

Anti thyroglobulin AB +
Antu TPO +
lymphs and plasma cells on FNA
eosinolphiles with granules- Hurthle cells

Front 42

what are hurthle cells

Back 42

eosinophiles with granular cytoplasm- seen in hashimoto hypothyroid

Front 43

whats DeQuervain thyroiditis

Back 43

aka subacute GRANULOMATOUS thyroiditis
not common, seen in women with genetics after viral URI

neck pain, worse with swalloq, radiates to jaw

GIANT CELLS, lymphs, plasma cells

Front 44

whats subacute lymphocytic thyroiditis

Back 44

PAINLESS (contrast to the granulomatous which is tender)

Front 45

what disease has giant cells in thyroid

Back 45

its subacute GRANULOMATOUS thyroiditis- deQuervian

can see neck pain and pain on swallow

Front 46

This 34 y/o female c/o sudden onset of severe
pain in the area of the thyroid 3 days after
contracting an URI. The pain radiated to the
angles of her jaw bilaterally. She also c/o
malaise, sweats and myalgias.
• PE: patient anxious and hyperkinetic, temp. 38.6
(101.5F) pulse 122. Thyroid mildly, diffusely
enlarged and exquisitely tender to palpation.
• What is the likely diagnosis

Back 46

subacute Granulomatous thyroiditis, deQuervian

tender, contrast to the painless (lymphocytic thyroiditis)

Front 47

whats riedel thyroiditis

Back 47

fibrosis of thyroid

associated with other causes of fibrosis

Front 48

fibrosis

giant cells

Back 48

fibrosis- reidel

giant cells- granulomatous, deQuervain

Front 49

types of goiter and associations

Back 49

toxic- hyperthyroidism

Non Toxic
Simple- endemic (iodine deficit in population) or sporadic *young females)
Multinodular

Front 50

if you habve a non toxic goiter, whats the metaabolic state

Back 50

toxic goiter- HYPERthyroid

Front 51

what are hte consequences and complications of goiters

Back 51

plummer syndrme

Front 52

A 67‐year‐old woman presented with a 6‐mon.
history of dyspnea and dysphagia. Physical
examination revealed a small, low cervical
goiter with nonpalpable lower poles.
The serum thyrotropin and free thyroxine levels
were normal.
What is the clinical diagnosis of these findings

Back 52

multinodular goiter

Front 53

what are hte clinical pearls about thyroid nodule

Back 53

1. solitary more likely to be CA then muttinodule

2. nodule in youg more likely to be CA

3. nodule in male more likely to be CA than in female

4. hx of radiation increased risk of thyroid CA

5. nodules that take I more likely to be benign

Front 54

we have a 25 yo male with a multinodule.

Back 54

CA
single lesion
younger pt
male
neck radiation hx
nodules take up I

NOT CA
multinodule
old pt
female

Front 55

thyroid adenomas are derived from...

Back 55

follicular epithelium

Front 56

are adenomas assocated with CA usually

prognosis

Back 56

nope

Front 57

what path is important in adenoma pathogenesis

Back 57

chronic cAMP signal --> growth advantage

Front 58

adenoma gross and micro

Back 58

single encapsulated lesion