Plab 1 Lectures Endo Notes

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Riedel thyroiditis, or Riedel's thyroiditis (RT), is a rare, chronic inflammatory disease of the
thyroid gland characterized by a dense fibrosis that replaces normal thyroid parenchyma.
The fibrotic process invades adjacent structures of the neck and extends beyond the
thyroid capsule. This feature differentiates RT from other inflammatory or fibrotic disorders
of the thyroid. Extension beyond the thyroid also differentiates this from the fibosing
variant of Hashimoto thyroiditis.
Involvement in RT may be unilateral or bilobar. Thyroid function depends on the extent to which the
normal thyroid gland has been replaced by fibrotic tissue. Most patients are euthyroid,
but hypothyroidism is noted in approximately 30% of cases. Rarely, hyperthyroidism can occur, but
this is probably secondary to a coexisting condition. (See Prognosis, Presentation, and Workup.)
Some experts have traditionally believed that RT is not primarily a thyroid disease but rather that it is
a manifestation of the systemic disorder multifocal fibrosclerosis. Approximately one third of RT cases
are associated with clinical findings of multifocal fibrosclerosis at the time of diagnosis.
In 1883, Professor Bernhard Riedel first recognized the disease. He published a
description of 2 cases in 1896 and of a third case in 1897. [1] Riedel used the
term eisenharte struma to describe the stone-hard consistency of the thyroid gland and its
fixation to adjacent structures. He noted the presence of chronic inflammation with fibrosis
and the absence of malignancy on microscopic examination. Simple wedge resection of
the thyroid isthmus was used to alleviate tracheal obstruction and is still the preferred
surgical therapy for RT.
Complications
Because of the encroachment beyond the thyroid capsule, nonthyroid problems can be associated
with RT. Complications of Riedel thyroiditis can include the following:
• Airway obstruction
• Dysphonia
• Hoarseness - Due to recurrent laryngeal involvement
• Hypothyroidism
• Hypoparathyroidism
• Dysphagia
• Stridor - Due to tracheal compression
• One distinguishing feature of Riedel thyroiditis (RT) is the absence of associated cervical
adenopathy. However, accurate diagnosis of RT requires open biopsy. [12]
• Imaging studies may suggest a diagnosis of RT, but findings can be nonspecific. The
laboratory findings in RT are also nonspecific. The erythrocyte sedimentation rate (ESR) is
generally elevated. Most patients remain euthyroid, but approximately 30% of patients become
hypothyroid. Rarely, patients are hyperthyroid.
• Although clinical features of RT closely resemble those of anaplastic carcinoma of the thyroid,
RT and anaplastic carcinoma can be distinguished from each other by immunohistochemistry.
• In one review, antithyroid antibody levels (TG-Ab and TPO-Ab) were found to be elevated in
67% of 178 cases of Riedel thyroiditis. [3] However, it is not certain whether such
autoantibodies are pathogenic or whether their presence merely reflects exposure of the
immune system to sequestered antigens released by the fibrotic destruction of normal thyroid
parenchyma.

Radioiodine is less expensive and has a lower complication rate than surgery and may be preferred as
definitive therapy of hyperthyroidism in nonpregnant patients except in patients with moderate or severe
orbitopathy. For patients with significant symptoms of hyperthyroidism, who are older, or who have underlying
heart disease or other comorbidities, we treat with a thionamide (in addition to beta blockers) to restore
euthyroidism prior to radioiodine treatment. For patients with mild, well-tolerated hyperthyroidism, there is no
need to pretreat with a thionamide, and radioiodine can be given soon after the diagnosis is made. Firstly,
since radioiodine treatment carries a substantial risk of exacerbating pre-existing thyroid eye disease it
should be avoided as far as possible in patients with active or severe ophthalmopathy, in whom medical
therapy with a thionamide drug such as carbimazole is preferable.
Aplasia cutis congenita is a condition in which there is congenital (present from birth) absence of skin, with
or without the absence of underlying structures such as bone
Omphalocele the infant's intestines, liver, or other organs stick outside of the belly through the belly button.
The organs are covered in a thin, nearly transparent sac that hardly ever is open or broken.

Birefringence is formally defined as the double refraction of light in a transparent, molecularly ordered
material, which is manifested by the existence of orientation-dependent differences in refractive index.

Propylthiouracil and Carbimazole the action is to serve as substrate for thyroid peroxidase (TPO) and
inhibits it and decreases incorporation of iodide into tyrosine molecules.

Prolactinoma: a benign tumor (adenoma) of the pituitary gland that produces prolactin
Investigation
• Always exclude other causes of prolactinemia
• Serum prolactin < 2000mU/L  Microprolactinoma OR a non-functioning macroadenoma compressing the
pituitary stalk
• Serum prolactin > 4000mU/L  Macroprolactinoma may cause visual symptoms (bitemporal
hemianopia) due to compression of optic chiasm
• MRI
Management
• Drug treatment should always be tried first
• Cabergoline is more effective than bromocriptine with fewer side effects
• Microadenoma < 10mm: Cabergoline / bromocriptine only
• Macroadenoma > 10mm: Drugs + Trans-sphenoidal surgery
• Surgery is needed when failing to respond to medical treatments with persisting visual symptoms (uni- or
bitemporal hemianopia) or pressure effects
One of the main regulators of the production of prolactin from the pituitary gland is the hormone called
dopamine, which is produced by the hypothalamus, the part of the brain directly above the pituitary

gland. Dopamine restrains prolactin production, so the more dopamine there is, the less prolactin is
released.
One of the main regulators of the production of prolactin from the pituitary gland is the hormone called
dopamine, which is produced by the hypothalamus, the part of the brain directly above the pituitary
gland. Dopamine restrains prolactin production, so the more dopamine there is, the less prolactin is
released. Dopamine serves as the major prolactin-inhibiting factor or brake on prolactin secretion. Dopamine
is secreted into portal blood by hypothalamic neurons, binds to receptors on lactotrophs, and inhibits both the
synthesis and secretion of prolactin.
MOA of dopamine agonists:
1. Suppress prolactin with normalization of gonadal functions and terminates galactorrhea
2. Shrink the tumor and restore other hormonal axes
3. Correct visual field defect by chiasmal decompression thus immediate surgical decompression is not
Indicated

Small cell lung cancer causes: Hyponatremia due to SIADH + Hypokalemia (increased mineralocorticoid activity)
• Tumor in the diencephalon  DI

• Tumor in the cerebrum/cerebellum  SIADH
Management of SIADH
- Treat the cause and restrict fluid
- If severe ➝ Salt + loop diuretics
- Vaptans (Vasopressin receptor antagonist)
- Demeclocycline, used rarely
Diabetes insipidus
1. Cranial DI: due to low ADH  inability to concentrate urine  polyurea and polydipsia
- Could be due to metastasis to the Diencephalon (contains hypothalamus)
2. Nephrogenic DI: inability to concentrate urine due to resistance to ADH in the kidney

Acromegaly:
In acromegaly there is excess growth hormone secondary to a pituitary adenoma in over 95% of cases. A minority of
cases are caused by ectopic GHRH or GH production by tumors e.g. pancreatic
Features
• coarse facial appearance, spade-like hands, increase in shoe size
• large tongue, prognathism, interdental spaces
• excessive sweating and oily skin
• features of pituitary tumor: hypopituitarism, headaches, bitemporal hemianopia
• raised prolactin in 1/3 of cases → galactorrhea
• 6% of patients have MEN-1

Investigations
• GH levels tend to vary during the day  unreliable and not recommended
• Best initial → Insulin like growth factor (IGF-1), used as screening and monitoring
• Most definitive → OGTT with serial growth hormone measurements
- normally, GH is usually suppressed with glucose
- in acromegaly, there is no suppression of growth hormone with glucose
• MRI may show a tumor. MRI scan is more sensitive than CT
Complications
• hypertension
• diabetes (>10%)
• cardiomyopathy
• colorectal cancer
Management:
• Trans-sphenoidal surgery
• Somatostatin analogue (GH-inhibiting hormone)
• Dopamine-agonists (cabergoline, bromocriptine)
• Pegvisomant
The insulin tolerance test has been used to distinguish Cushing’s syndrome from
pseudo-Cushing’s states. Serum cortisol values increase in normal people after
acute hypoglycemia, presumably because of central stimulation of CRH
and vasopressin. The sustained hypercortisolism of Cushing’s syndrome
suppresses CRH and vasopressin secretion and so blunts this response. The
CRH/vasopressin neurons are presumed to be overactive in pseudo-Cushing’s
states, particularly those that are depression associated, so a normal response to
hypoglycemia (<40 mg/dL; <2.2 nmol/L) is usually maintained. Unfortunately,
approximately 18% of patients with Cushing’s syndrome, especially those with
minimal hypercortisolism, show a normal response to adequate hypoglycemia.

•

Emergency administration of fludrocortisone is not required because high-dose
hydrocortisone has a mineralocorticoid effect.
Pheochromocytoma
• Rare catecholamine secreting tumor
• Rule of 10%  10% bilateral, 10% malignant, 10% extra-adrenal (MC site – organ of Zuckerkandl, adjacent to
the bifurcation of the aorta), 10% familial (may be associated with MEN type II, neurofibromatosis and von
Hippel-Lindau $), 10% not associated with hypertension
• PHeochromocytoma  Palpitations, Headaches, PHlushing
• Investigation  24h collection of metanephrines
• Management  Surgery, but the patient must be stabilized first
- Alpha-blocker (phenoxybenzamine)  must be given before beta-blocker
- Beta-blocker (propranolol)
• Alpha and beta blockade are used to control blood pressure and prevent intraoperative hypertensive crisis
• Alpha blockade is given 7-10 days before operation to allow expansion of the blood volume, if beta blockade
started too soon, unopposed alpha stimulation can precipitate a hypertensive crisis

Hypokalemia. Although equally dangerous, hypokalemia is less common in CKD patients, as impaired renal
K excretion usually leads to hyperkalemia. CKD patients can, however, still develop hypokalemia due
to gastrointestinal K loss from diarrhea or vomiting or renal K loss from non-K-sparing diuretics.
DKA is a well-known cause of hypokalemia caused by osmotic diuresis leading to a total body potassium
deficiency of 3 to 6 mEq/kg. At presentation, potassium levels are typically “normal” due to the extracellular
shift of potassium (K+) from insulin deficiency and acidosis
In SCLC, amongst the important causes of low potassium levels in the blood are adrenocorticotrophic
hormone (ACTH)-secreting tumors.

• Insulin stimulates intracellular reuptake of K+ and glucose is given to prevent hypoglycemia
• After Insulin and glucose infusion, blood glucose is monitored after 15 mins, 30 mins and
then hourly for the next 6 hours due to fear of late hypoglycemia. Shifting K+ intracellularly doesn’t reduce total body
K+, and after 2-6 hours, there’s an efflux of K+ back into the extracellular space
resulting in serum levels as high or sometimes higher than at the outset. Therefore, any of these steps should be
combined with attempting to reduce total body K+. This can be done by:
• Avoiding medications that raise K+
• Promote urinary K+ loss
- IV fluid as long as the patient is not significantly overload. Renal excretion is enhanced easily in patients with
normal kidney function by administering IV saline accompanied by a loop diuretic
- if well hydrated, consider starting on increasing the dose of a loop diuretics (frusemide)
• Remove excess K+
- Ca resonium has a slow onset of action (at least 2-6hours)
• Dialysis
- if hemodialysis is performed within 15-30 mins then treatments to move K+ into cells are unlikely to be
helpful and may make K+ removal on dialysis more difficult

Magnesium helps transport calcium and
potassium ions in and out of cells. It may also contribute to the absorption of these important minerals. This is
why a lack of magnesium can lead to low calcium and potassium levels.

Concomitant magnesium deficiency aggravates hypokalemia and renders it refractory to treatment by
potassium

K+ is passively transported along its concentration gradient through a K+ leak channel in the apical aspect of the
cells, back into the lumen of the ascending limb. This K+ "leak" generates a positive electrochemical
potential difference in the lumen. This drives more paracellular reabsorption of Na+, as well as other cations such
as magnesium (Mg2+) and importantly calcium Ca2+ due to charge repulsion.

CAH can occur in various forms.Classical forms appear in infancy, and non-classical forms appear in late childhood. The
presentation in patients with classic CAH can be further subdivided into two forms: salt-wasting and simple-virilizing,
the development of male physical characteristics (such as muscle bulk, body hair, and deep voice) in a
female or precociously in a boy, typically as a result of excess androgen production. depending on whether
mineralocorticoid deficiency presents or absents, respectively.
Classic
Salt-wasting
In 75% of cases of severe enzyme deficiency, insufficient aldosterone production can lead to salt wasting, failure to
thrive, and potentially fatal hypovolemia and shock. A missed diagnosis of salt-loss CAH is related to the increased risk of
early neonatal morbidity and death.

Tertiary hyperparathyroidism means excess production of parathyroid hormone that has escaped all
normal body feedback controls and so persists even in cases where the initial cause (low blood calcium) has
been corrected.
In secondary hyperparathyroidisrn, the serum calcium is normal and the PTH level is elevated. Tertiary
hyperparathyroidism is characterized by excessive secretion of PTH after longstanding secondary
hyperparathyroidism. in which hypercalcemia has ensued.

Diabetes Mellitus

Repaglinide is a nonsulfonylurea, oral hypoglycemic agent used in the treatment of type 2 diabetes
mellitus and was the first of the meglitinide analogs to be marketed.

Repaglinide lowers blood glucose levels by stimulating the release of insulin from the
pancreas.
Lipodystrophy cause a person to lose fat from some parts of the body There may be a notable absence
of fat under the skin and this can be associated with the increased prominence of muscles and blood vessels

Your pancreas needs the enzyme glutamic acid decarboxylase (GAD) to function
normally. Antibodies that target this enzyme are called GAD antibodies.
C-Peptide, a marker for insulin secretion, is purported to be elevated in patients with insulinoma C-peptide levels
of 2 nmol/L or greater usually indicate insulinoma.

Hyperphosphtemia may be seen in critical illness and in patients who have ingested phosphate-containing
enemas. Phosphate binds calcium avidly, causing acute hypocalcemia. Acute hypocalcemia secondary to
hyperphosphatemia may also result from renal failure or excess tissue breakdown because of rhabdomyolysis
or tumor lysis.
In acute hyperphosphatemia, calcium is deposited mostly in the bone but also in the extraskeletal tissue. In
contrast, in chronic hyperphosphatemia, which is nearly always from chronic renal failure, calcium efflux from

the bone is inhibited and the calcium absorption is low, because of reduced renal synthesis of 1,25-
dihydroxyvitamin D. However, other consequences of renal failure, including a primary impairment in calcitriol
synthesis, also contribute to hypocalcemia.
A combination of increased calcium input into the extracellular space and reduced calcium removal by the
kidney accounted for the hypercalcemia in addison’s disease. The mechanisms responsible for the reduction
in calcium removal were decreased glomerular filtration and increased tubular calcium reabsorption. Both
renal factors were secondary to volume depletion and improved rapidly during rehydration with saline
infusion.
Thyroid hormones are known to cause bone resorption and mobilizing calcium from bone to circulation
leading to hypercalcemia. High levels of interleukin-6 (IL-6) seen in hyperthyroidism stimulates osteoclastic
activity

alfacalcidol is more effective than vitamin D3 in increasing bone mass Alfacalcidol, or 1-alpha-
hydroxycholecalciferol or 1-alpha-hydroxyvitamin D3, is a non-endogenous analogue of vitamin D. It plays
an essential function in calcium homeostasis and bone metabolism.

Corrected calcium (mg/dL) = measured total Ca (mg/dL) + 0.8 (4.0 - serum albumin [g/dL]),
where 4.0 represents the average albumin level


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• Tumor in the diencephalon  DI

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