Endocrinology: Pituitary,hypothalamus, Thyroid Flashcards

1
Q

What are the causes of hyperprolactenemia

A
I. Physiologic hypersecretion
Pregnancy
Lactation
Chest wall stimulation
Sleep
Stress    
   II. Hypothalamic–pituitary stalk damage
Tumors
Craniopharyngioma
Suprasellar pituitary mass
Meningioma
Dysgerminoma
Metastases
Empty sella
Lymphocytic hypophysitis
Adenoma with stalkCompression
Granulomas
Rathke’s cyst
Irradiation
Trauma
Pituitary stalk section
Suprasellar surgery 

III. Pituitary hypersecretion
Prolactinoma
Acromegaly

IV. Systemic disorders
Chronic renal failure
Hypothyroidism
Cirrhosis
Pseudocyesis
Epileptic seizures 

V. Drug-induced hypersecretion

Dopamine receptor blockers
Atypical antipsychotics: risperidone
Phenothiazines: chlorpromazine, perphenazine
Butyrophenones: haloperidol
Thioxanthenes
Metoclopramide

Dopamine synthesis inhibitors
α-Methyldopa

Catecholamine depletors
Reserpine

Opiates

H2 antagonists
Cimetidine, ranitidine

Imipramines
Amitriptyline, amoxapine

Serotonin reuptake inhibitors
Fluoxetine

Calcium channel blockers
Verapamil

Estrogens

Thyrotropin-releasing hormone

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2
Q

Most common pituitary hormones hypersecretion syndrome in both men and women

A

Hyperprolactenemia

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3
Q

C/f of person with hyperprolactenemia

A
WOMEM
amenorrhoea
Galactorrhoea
Infertility
Dec mineral bone density(chronic as it causes hypoestronegism)

Hypoestronigism
Dec libido
Wt gain
Mild hirusitism

MEN
Hyperprolacteniema
Dec libido
Infertilty
Visual loss
True galactorrhoea: uncommon
Reduced testosterone
.Oligospermia
.Osteoporosis
.Reduced muscle mass
.Dec beard growth
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4
Q

Mainstay of treatment for cushings ds

A

Selective transphenoidal resection

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5
Q

Kallman syndrome

A

Kallmann syndrome results from defective hypothalamic gonadotropin-releasing hormone (GnRH) synthesis and is associated with anosmia or hyposmia due to olfactory bulb agenesis or hypoplasia .

Prevents progression through puberty.
Dec LH,FSH, estrogen,testosterone

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6
Q

Postpartum women with hyperprolactenemia and prominent pituitary mass

A

Can be Lymphocytic hypophysitis

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7
Q

Empty sella

A
Empty/partial empty
Ass with inc ICP
Normal pituitary fxn(rim present)
Hypopotuitarism can also develop insidiously
Can be result of silent infarction
Filled by CSF
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8
Q

Pituitary apoplexy

A

Acute intrapituitary haemorrhagic vascular event

CAUSES
Pituitary apoplexy may occur spontaneously in a preexisting adenoma; postpartum (Sheehan’s syndrome); or in association with diabetes, hypertension, sickle cell anemia, or acute shock.

RX
High dose glucocorticoids:
Patients with no evident visual loss or impaired consciousness

Surgical decompression: significant or progressive visual loss, cranial nerve palsy, or loss of consciousness

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9
Q

Laron syndrome

A

GH insensitivity due to mutation in GH receptor.

Normal/ high GH levels
Low IGF-I levels

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10
Q

Sequential loss of hormone loss in adult GH defeciency

A

The sequential order of hormone loss is usually GH → FSH/LH → TSH → ACTH

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11
Q

IGF-I measurements provide a useful index of therapeutic responses but are not sufficiently sensitive for diagnostic purposes. Why

A

Because its level may be normal on GH def.

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12
Q

Contraindications to GH therapy

A

active neoplasm
intracranial hypertension
uncontrolled diabetes
retinopathy

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13
Q

Therapy in gonadotropin deficiency

A

MALES
Testosterone
GnRH therapy, gonadotropin: if infertility

FEMALES
Estrogen
Progesterone
GnRH , gonadotropin : infertility

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14
Q

Features of sellar mass lesions

A

*Pituitary

Hypogonadism
Hypothyroidism
Growth failure and adult hyposomatotropism
Hypoadrenalism

*Optic chiasm

Loss of red perception
Bitemporal hemianopia
Superior or bitemporal field defect
Scotoma
Blindness

*Hypothalamus

Temperature dysregulation
Appetite and thirst disorders
Obesity
Diabetes insipidus
Sleep disorders
Behavioral dysfunction
Autonomic dysfunction

*Cavernous sinus

Ophthalmoplegia with or without ptosis or diplopia
Facial numbness

Frontal lobe
Personality disorder
Anosmia

*Brain

Headache
Hydrocephalus
Psychosis
Dementia
Laughing seizures
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15
Q

Stalk section phenomenon of pituitary lesion

A

May compress portal vessels

Disrupting pituitary acess to hypothalamic hormones and dopamine

Leading to dec in all pituitary hormones except prolactin

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16
Q

Physiologic pituitary enlargement seen in

A

Adolocent

Pregnancy

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17
Q

PRL suppression by dopamine agonists does not necessarily indicate that the underlying lesion is a prolactinoma.why

A

hyperprolactinemia caused secondarily by the mass effects of nonlactotrope lesions is also corrected by treatment with dopamine agonists despite failure to shrink the underlying mass

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18
Q

mainstay of therapy for patients with micro- or macroprolactinomas

A

Oral dopamine agonists

Not Sx/radiation

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19
Q

Dopamine agonist used in pituitary prolactinoma

A

Cabergoline: long acting

Bromocriptine: short acting , so used in PREGNANCY

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20
Q

Men tend to present with larger prolactinoma tumors than women.why

A

Because features of male hypogonadism are less readily evident

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21
Q

Causes of acromegaly

A

*Excess GH

PITUITARY
adenoma
Men1
Mc cune albright

EXTRA PITUITARY
Pancreatic islet cell
Lymphoma

*excess GHRH
Central: hypothalamic hamartoma, christoma
Peripheral: carcinoid of chest/abdomen(MOST COMMON CAUSE OF HIGH GHRH)
Small cell lung ca
Adrenal adenoma
Medullary thyroid ca
Pheochromocytoma

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22
Q

Features of acromegaly

A

Acral bony overgrowth :
frontal bossing
increased hand and foot size
mandibular enlargement with prognathism
widened space between the lower incisor teeth
In children and adolescents, initiation of GH hypersecretion before epiphyseal long bone closure is associated with development of pituitary gigantism

 Soft tissue:
 increased heel pad thickness
Increased shoe or glove size
ring tightening
characteristic coarse facial features
 large fleshy nose
 Generalized visceromegaly : 
 cardiomegaly
macroglossia
thyroid gland enlargement.
Upper airway obstruction

DM

colonic malignancy

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23
Q

________of GH-secreting adenomas is the initial treatment for most patients

A

Surgical resection

Not medical(only if sx fails)

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24
Q

Medical Rx in GH adenoma

A
SOMATOSTATIN ANALOGUES(dec GH so dec IGF)
Acts via somatostatin SST receptor which are expressed over GH secreting tumor

octreotide
Lanreotide
S/E
Git: Transient nausea, abdominal discomfort, fat malabsorption, diarrhea, and flatulence.
Cholesterol gallstones/sludge(due to dec gb motility)

GH RECEPTOR ANTAGONIST(dec IGF ,GH remain elevated)
pegvisomant

DOPAMINE AGONIST
Suppress GH secretion

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25
Q

CF of cushing syndrome

A
Obesity or weight gain (>115% ideal body weight)
 Thin skin 
Moon facies 
Hypertension 
Purple skin striae 
Hirsutism 
Menstrual disorders (usually amenorrhea) Plethora 
Abnormal glucose tolerance 
Impotence 
Proximal muscle weakness 
Truncal obesity
 Acne 
Bruising 
Mental changes 
Osteoporosis 
 Edema of lower extremities Hyperpigmentation 
Hypokalemic alkalosis 
Diabetes mellitus
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26
Q

Use of inferior petrosal venous sampling in cushing syndrome

A

Diatinguish bw pituitary ACTH producing adenoma from ectopic ACTH producing tumor

Level of ACTH is measured in IPS and peripheral veins in response to CRH

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27
Q

RX OF CHOICE FOR CUSHING DS

A

selective transsphenoidal resection

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28
Q

Drugs used in cushing syndrome

A

SOMATOSTATIN ANALOGUE
Pasireotide
S/e: diabetes ( supressed pancreatic secretion of insulin ,incretins) rest git

GLUCOCORTICOID RECEPTOR ANTAGOINIST
Mefiprostone

STEROIDOGENIC INHIBITORS
Metyrapone( inhibitis and 11b-hydroxylase)
Ketaconazole(inhibits CYP 450)

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29
Q

Nelson syndrome

A

Adrenalectomy in the setting of residual corticotrope adenoma tissue.

characterized by rapid pituitary tumor enlargement and increased pigmentation secondary to high ACTH.

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30
Q

Most common type of pituitary adenoma

A

Nonfunctional

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31
Q

Moa of AVP

A

V2 receptors- G protein- adenylate cyclase -inc cAMP- more insertion of AQP2

V1 receptors-phospholipase C- contraction of smooth muscle in blood vessels in the skin and gastrointestinal tract,

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32
Q

Drugs caused DI

A
Lithium
Demeclocycline
Methoxyflurane
Amphotericin 
Aminoglycosides
Cisplatin
Rifampin
Foscarnet
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33
Q

Causes of hyppnatremia due to inapprropriate diuresis

A

three different types of salt and water imbalance:

(1) an increase in total body water that exceeds the increase in total body sodium (hypervolemic hyponatremia)
Causes: CHF, cirrhosis , nephrosis

(2) a decrease in body sodium greater than the decrease in body water (hypovolemic hyponatremia)
Causes:diarrhoea , diuretic abuse, mineralocorticoid deficiency

(3) an increase in body water with little or no change in body sodium (euvolemic hyponatremia)
Cause: * nausea, cortisol deficiency
* SIADH

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34
Q

Level of AVP in all 3 types of hyponatremia due to inapp diuresis

A

Increased in all

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35
Q

Treatment of DI

A

PITUITARY DI
Desmopressin

NEPHROGENIC DI
Thiazide diutetics, amiloride
Low Na diet , PG synthsesis inhibitor

PRIMARY POLYDYPSIA
No way to correct
Desmopressin, antidiuretic will cause water intoxication because it does not inhibit urge to drink

V2 RECEPTOR MUTATION

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36
Q

Types of primary polydypsia

A

DYPSOGENIC
characterized by inappropriate thirst caused by a reduction in the set of the osmoregulatory mechanism. It sometimes occurs in association with multifocal diseases of the brain such as neurosarcoid, tuberculous meningitis, and multiple sclerosis but is often idiopathic

PSYCHOGENIC POLYDYSIA
is not associated with thirst, and the polydipsia seems to be a feature of psychosis or obsessive compulsive disorder

IDIOPATHIC
results from recommendations to increase fluid intake for its presumed health benefits

37
Q

Effect of estrogen on TBG as in pregnancy /OCP

A

Increase TBG
Inc total T3 and T4
But free T3 and T4 normal

Androgens,: dec

38
Q

Why the dose of throxine has to be increased in pregnancy?

A

Because the free thyroxine binds to TBG(as it is raised idue to effect of estrogen)which can cause hypothyroidism

39
Q

Pendrin

A

A protein responsible for efflux of iodine in the follicle

40
Q

Gestational DI

A

A primary deficiency of plasma AVP also can result from increased metabolism by an N-terminal aminopeptidase produced by the placenta. It is referred to as gestational DI because the signs and symptoms manifest during pregnancy and usually remit several weeks after delivery

41
Q

Why is there no hypernatremia and other overt physical or laboratory signs of dehydration in patient with central/nephrogenic DI

A

increase in plasma osmolarity and sodium will stimulates thirst and a compensatory increase in water intake.

hypernatremia and other overt physical or laboratory signs of dehydration do not develop unless the patient also has a defect in thirst or fails to increase fluid intake for some other reason.

42
Q

Types of deiodinases

A

DEIODINASE 1
low affinity for T4

DEIODINASE 2
Converts T4 to T3

DEIODINASE 3
Inactivates T4 and T3

43
Q

Thyroid act on cytoplasmic/nuclear receptor

A

Nuclear though it is a peptide

44
Q

Most common cause of preventanle.mental deficiency

A

Iodine deficiency

45
Q

Cause of creatinism

A

Congenital hypothyroidism

Thyroid hormone synthesis normally begins at about 11 weeks of gestation. If there is no thyroid gland/hormone mothers thyroid will compensate till birth so chances creatinism will be in first few yrs of life.

If mother is also hypothyroid during pregnancy the child will be born with creatinism.

46
Q

Like other pituitary hormones, TSH is released in a pulsatile manner and exhibits a diurnal rhythm; its highest levels occur at night but still we do single measurement. Why?

A

TSH excursions are modest in comparison to those of other pituitary hormones, in part, because TSH has a relatively long plasma half-life (50 min)

47
Q

Wolff chaikoff effect

A

Excess iodide transiently inhibits thyroid iodide organification

48
Q

cause of inc and dec in TBG

A
INCREASE TBG: inc in estrogens
Pregnancy
OCP
Hormone therapy
Tamoxifen
Serm
Inflammatory liver ds

DECREASE TBG
Androgens
Nephrotic syndrome

49
Q

Serum Tg levels are increased in all types of thyrotoxisosis except

A

Thyrotoxicosis factitia

Caused by self administration of thyroid hoemones

50
Q

Function of TPO in thyroid hormone synthesis

A

Oxidation of iodide to iodine

Coupling of MIT/DIT and DIT/DIT

51
Q

Antibodies which can be found in hypothyroidism

A

TPO
Tg
TSH-R(blocking ,not stimulatory like TSI)

iseful markers of autoimmunity

52
Q

Caise myxedema in hypothroidism

A

Increased dermal glycosaminoglycan content traps water, giving rise to skin thickening without pitting (myxedema)

53
Q

Symptoms of hypothroidism

A

SYMPTOMS
Tiredness
weakness
Dry skin
Feeling cold
Hair loss
Difficulty concentrating and poor memory Constipation
Weight gain with poor appetite (due to fluid retention)
Dyspnea(dec ventilation ,muscle weakness)
Hoarse voice (tissue deposition)
Menorrhagia (later oligomenorrhea or amenorrhea)
Paresthesia
Impaired hearing (fluid accumulation)

SIGNS
 Dry coarse skin
 cool peripheral extremities (blood flow directed away from skin due to inc PVR)
Puffy face,hands, and feet   (myxedema) Diffuse alopecia 
Bradycardia
 Peripheral edema 
Delayed tendon reflex relaxation 
Carpal tunnel syndrome 
Serous cavity effusions
54
Q

Effect of hypothroidism on CVS

A

Dec in SV
Inc in PVR
So, Hypertension particularly diastolic

55
Q

Causes of hypothyroidism

A

PRIMARY
Autoimmune hypothyroidism:
Hashimoto’s thyroiditis
atrophic thyroiditis

Iatrogenic:
131I treatment
subtotal or total thyroidectomy
external irradiation of neck for lymphoma or cancer

Drugs:
iodine excess (including iodine-containing contrast media and amiodarone)
lithium
antithyroid drugs
p-aminosalicylic acid
interferon α and other cytokines, aminoglutethimide
tyrosine kinase inhibitors (e.g., sunitinib)

Congenital hypothyroidism:
absent or ectopic thyroid gland dyshormonogenesis
TSH-R mutation

Iodine deficiency

 Infiltrative disorders
 amyloidosis
 sarcoidosis
 hemochromatosis
 scleroderma
cystinosis
Riedel’s thyroiditis

Overexpression of type 3 deiodinase in
infantile hemangioma and other tumors

TRANSIENT
Silent thyroiditis, including postpartum thyroiditis
Subacute thyroiditis
Withdrawal of supraphysiologic thyroxine treatment in individuals with an intact thyroid

After 131I treatment or subtotal thyroidectomy for Graves’ disease

SECONDRY
Hypopituitarism:
 tumors
pituitary surgery 
 irradiation
infiltrative disorders
Sheehan’s syndrome
trauma
 genetic forms of combined pituitary hormone deficiencies
 Isolated  TSH deficiency or inactivity Bexarotene treatment 
Hypothalamic disease: 
tumors
trauma
infiltrative disorders
idiopathic
56
Q

Myxedema coma

A

Long standing hypothyroidism
Patient took no medication

S/s
Bradycardia
Hypotension
Hyoothermia
Stupor
Coma
Seizures
Delayed deep tendon reflex
Other feature of hypothyroidism

PRECIPITATING FACTORS
Myxedema coma almost always occurs in the elderly and is usually precipitated by factors that impair respiration, such as drugs (especially sedatives, anesthetics, and antidepressants), pneumonia, congestive heart failure, myocardial infarction, gastrointestinal bleeding, or cerebrovascular accidents. Sepsis should also be suspected. Exposure to cold may also be a risk factor.

TREATMENT
Iv.bolus of levothyroxine

Liothyronine(T4 to T3 conversion is impaired in myxedema , but high dose can cause artythmia)

Hydrocortisone(due to impaired adrenal reserve)

Treat precipitating factor

57
Q

Why T3 is not used in long term thyroid replacement

A

Due to short half life

3 -4 daily doses have to be given leading to fluctuating T3 levels

58
Q

Causes of thyrotoxicosis

A
PRIMARY HYPERTHYROIDISM
Graves’ disease
 Toxic multinodular goiter
 Toxic adenoma
 Functioning thyroid carcinoma 
metastases
 Activating mutation of the  TSH receptor Activating mutation of GSα  (McCune-Albright syndrome)
 Struma ovarii 
Drugs: iodine excess (Jod-Basedow phenomenon) 

THYROTOXICOSIS WITHOUT HYPERTHYROIDISM
Subacute thyroiditis
Silent thyroiditis
Other causes of thyroid destruction: amiodarone, radiation, infarction of adenoma
Ingestion of excess thyroid hormone (thyrotoxicosis factitia) or thyroid tissue

SECONDRY HYPERTHYROIDISM
TSH-secreting pituitary adenoma
Thyroid hormone resistance syndrome: occasional patients may have features of thyrotoxicosis
Chorionic gonadotropin-secreting tumors Gestational thyrotoxicosisa

59
Q

Thyrotoxicoisis and hyperthyroidism

A

THYROTOXICOSIS
state of thyroid hormone excess

HYPERTHYROIDISM
Result of excessive throid function

60
Q

Antibodies in graves ds

A

TSI

TPO are also.present

61
Q

Can TSI cross placenta

A

Yes(not Ab Against TPO, Tg)

So can cause thyrotoxicosis in fetus.
Antityhroid drugs given to mother will protect the fetus also as they will also cross placenta

62
Q

Triad of graves ds

A
OPHTHALMOPATHY
eye sign
Grittiness
Tearing
Proptosis
Corneal damage
Periorbital edema
Scleral injection
Chemosis
Optic nerve compression

DERMOPATHY
Most frequent over ant and lateral aspects of lower leg
So aka Pretibial myxedema
Noninflamed indurated plaque

ACROPATHY
Form of clubbing

63
Q

Antithyroid drugs

A

Propylthiouracil
Carbimazole
Methimazole

MOA
All inhibit the function of TPO, reducing oxidation and organification of iodide.

These drugs also reduce thyroid antibody levels by mechanisms that remain unclear, and they appear to enhance rates of remission.

Propylthiouracil inhibits deiodination of T4 → T3.

64
Q

Which antithyroid drug prevent T4 to T3 conversion

A

Propylthiouracil

65
Q

Why propylthiouracil should not be given to children and pregnant

A

Hepatotoxicity

66
Q

Prevention of radioiodine induced thyrotoxic crises

A

Preadministeration of antithyroid drugs to decrease the hormone level but these drugs should be discontinued 3- 5 days before radionucleotide Rx because it will prevent its uptake and hence the effect

67
Q

RX of thyrotoxic crisis/ thyroid strom

A
S/s
Fever
Delerium
Seizures
Coma
Vomiting
Diarrhoea
Jaundice
Hyperthermia
Arrythmia
Cardia failure
PRECIPITATING FACTORS
acute illness (e.g.,  stroke, infection, trauma, diabetic ketoacidosis), surgery (especially on the thyroid), or radioiodine treatment  of  a  patient  with  partially  treated  or  untreated  hyperthyroidism. 

DRUGS

Propylthiouracil(DOC: inhibit T4 to T 3 conversion)

If not available: methimazole

Iodine :block thyroid hormone synthesis via the Wolff-Chaikoff effect (the delay allows the antithyroid drug to prevent the excess iodine from being incorporated into new hormone)

Propanolol,esmolol (adrenergic manifestations, also prevent T4 to T3 conversion)

68
Q

Sign and symptoms of thyrotoxicoosis

A
SYMPTOMS
 Hyperactivity
 irritability
 dysphoria
Heat intolerance
 sweating
 Palpitations 
Fatigue and weakness 
Weight loss with increased appetite Diarrhea
 Polyuria (hypercalciuria)
Oligomenorrhea, 
loss of libido 
Insomnia
SIGNS
Tachycardia
 atrial fibrillation
 Tremor 
Goiter
 Warm, moist skin 
Muscle weakness
proximal myopathy
Hyperreflexia
 Lid retraction, lag
 Gynecomastia
Osteopenia
Alopecia
69
Q

Effect of thyrotoxicosis on CVS

A

Sinus tachycardia

Palpitations

Inc SBP especially

Inc stroke vol(high output cardiac failure)
So, bounding pulse, widened pulse pressure, aortic systolic murmer)

Atrial fibrillation

70
Q

Acite thyroiditis

A
Suppurative
Rare
Thyroid pain
Fever
Dysphagia
Erythema
Systemic symptoms

Inc ESR
Inc WBC
Fna’neutrophils

71
Q

Factors altering thyroid fxn in pregnancy

A

1) the transient increase in hCG during the first trimester, which stimulates the TSHR (dec TSH and inc thyroid hormones leading to transient gestational hyperthyroidism)
(2) the estrogen-induced rise in TBG during the first trimester, which is sustained during pregnancy
(3) alterations in the immune system, leading to the onset, exacerbation, or amelioration of an underlying autoimmune thyroid disease
(4) increased thyroid hormone metabolism by the placenta
(5) increased urinary iodide excretion, which can cause impaired thyroid hormone production in areas of marginal iodine sufficiency

72
Q

Effect of amiodarone on thyroid fxn

A

Can cause both hypo/hyperthyroidism

INITIALLY,
Hypothyroidism due to wolf-chaikoff effect

THAN,
inhibitory effects on deiodinase activity and thyroid hormone receptor action become predominant.
Inc T4, dec T3 , inc rT3, inc TSH

SOMETIMES , jod-basedow phenomenon occurs:
Thyroid hormone synthesis becomes excessive as a result of inc iodine exposure due to underlying thyroid abnormality (graves, nodular goitre) that results in inc in iodine uptake
Wolf chaikoff effect will not occur

73
Q

Subacute thyroiditis

A

Aka de Quervain’s thyroiditis
granulomatous thyroiditis
viral thyroiditis.

CAUSE: virus

THREE DISTINCT PHASES

  1. thyrotoxic: inc Tg,thyroid hormones , dec TSH, dec Radioactive iodine uptake
  2. hypothyroid: low T3/T4 , inc TSH , inc RIU
  3. recovery
C/m
Pain
Refered to jaw, ear
Swelling
Fever
Features of thyrotoxicosis/hypothyroidism
H/o URT infection
Sore throat
Tender
TREATMENT
Aspirin large dose
Prednisone
B adrenergic blockers
No role of antityroid drugs in thyrotoxic state
74
Q

Silent thyroididis/painless thyroiditis/ postpartum thyroiditis (because mostly present in them)

A

3 differentiating feature from subacute thyroiditis are

  1. painless
  2. normal ESR
  3. positive TPO
75
Q

reidel thyroiditis

A
Insidious
Painless
Nontender
Hard
Asymmetric
Fixed
Local symptoms due to compression: 
Esophagus
Trachea
Neck veins
RLN

Dense fibrosis even outside thyroid capsule

CONFUSED WITH MALIGNANCY

76
Q

Sick euthyroid syndrome/nonthyroidal illness

A

Due to acute severe illness

Due to release of cytokines such as IL-6

Most common hormone pattern:
Low T3(total,free both)
Normal T4
Normal TSH

Cause:due to impaired peripheral conversion of T4 to T3 via 5’deiodination leading to inc rT3 and decreased clearance.
So inc production and dec clerance of rT3.

Help as:limit the catabolism in starved and ill patient

Very sick patients: dec in total T3 and T4 (low T4 syn)
Cause: accelerated degradation of T4 and T3
Altered binding to TBG

77
Q

Types of goitre

A

Diffuse nontoxic/simple/colloid goitre
No nodules and hyperthyroidism
Diffuse enlargement

Nontoxic multinodular goite

Toxic multinodular goitre(functional autonomy)

Hyperfunctioning solitary nodule/toxic adenoma

78
Q

Environmental goitrogens

A

cassava root, which contains a thiocyanate; vegetables of the Cruciferae family (known as cruciferous vegetables) (e.g., Brussels sprouts, cabbage, and cauliflower); and milk from regions where goitrogens are present in grass.

79
Q

Histological changes in nontoxic multinodular goitre

A
Variable nodule size
Hypercellular regions
Cystic areas filled with colloid
Fibrosis
Haemorrhage
Lymphocytic infilteration
80
Q

Sudden pain and haemorrhage in a nodyle is suggestive of

A

Malignancy

81
Q

Risk factors for thyroid ca

A

History of head and neck irradiation, including total-body irradiation for bone marrow transplant and brain radiation for childhood leukemia

Exposure to ionizing radiation from fallout in childhood or adolescence

Age <20 or >65 years

Increased nodule size (>4 cm)

New or enlarging neck mass

Male gender

Family history of thyroid cancer, MEN 2, or other genetic syndromes associ-ated with thyroid malignancy (e.g., Cowden’s syndrome, familial polypo-sis, Carney complex)

Vocal cord paralysis, hoarse voice

Nodule fixed to adjacent structures

Extrathyroidal extension

Lateral cervical lymphadenopathy

82
Q

Jod basedow effect

A

Enhanced thyroid hormone production by autonomous nodule(graves, toxic goitre) on giving contrast agents and other iodine containing substances

83
Q

Common Mode of spread of tumor cells in papillary and follicular thyroid ca

A

FOLLICULAR
Hematogenous

PAPILLARY
Lymphatic

84
Q

RET gene mutation seen in

A

Medullary ca of thyroid

85
Q

Types of medullary thyroid ca

A

SPORADIC

FAMILIAL
MEN 2A
MEN2B
Familial MTC without other features of MEN

86
Q

Characteritic histological findings in PTC

A

these include psammoma bodies, cleaved nuclei with an “orphan-Annie” appearance caused by large nucleoli, and the formation of papillary structures.

87
Q

Most common type of thyroid cancer

A

Papillary thyroid ca

88
Q

Why dx of follicular thyroid ca not possible on FNAC

A

FTC is difficult to diagnose by FNA because the distinc-tion between benign and malignant follicular neoplasms rests largely on evidence of invasion into vessels, nerves, or adjacent structures.

89
Q

Orphan annie nucleus

A

PTC