ENDOCRINE Flashcards

(35 cards)

1
Q

GnRH

A

Pulsatile administration of gonadotropin-releasing hormone (GnRH) stimulates FSH and LH release and is useful for the treatment of infertility.

Nonpulsatile (constant) infusion of GnRH, or a long-acting analog, suppresses FSH and LH release and subsequently suppresses gonadal function.
TX OF when suppression of gonadal function is desired, such as in certain patients with prostate cancer, endometriosis, precocious puberty, or premenopausal breast cancer.

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2
Q

TYROID DX

A

next cards

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3
Q

HYPERTHYRODISM

A

Graves disease is an autoimmune disorder triggered by thyrotropin receptor antibodies (TRAb) that bind and activate the TSH receptor. Serum TRAb immunoassays have a high sensitivity and specificity for Graves disease. HIGH BLOODV FLOW

The bone loss is driven by triiodothyronine, which stimulates osteoclast differentiation, increased bone resorption, and release of calcium.
(NOTE :Thyroid hormone NORMALLY stimulates osteoblast differentiation and activity, leading to increased formation of new bone)

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4
Q

THYROID ENZYMES

A

(INHIBITED BY PTU,B BLOCKER AND GLUCOCORTICOSTEROID)

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5
Q

subacute (granulomatous, de Quervain) thyroiditis

A

Elevated thyroid hormone, suppressed TSH (hyperthyroid phase)
Elevated serum thyroglobulin
Elevated ESR
Low radioiodine uptake (due to loss of TSH stimulation.)
diffuse enlargement of the gland with decreased blood flow on thyroid ultrasound.

ALWERYS REMEMBER Serum TSH is the most sensitive test for primary hypothyroidism.

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6
Q

Euthyroid sick syndrome

A

(low T3 syndrome) AND HIGH rT3

Clinical presentation

Abnormal thyroid function tests in acutely ill patient
Mild central hypothyroid state; asymptomatic

Pathophysiology

Suppression of 5’-deiodinase by glucocorticoids and inflammatory cytokines (eg, TNF-alpha, IL-1, IFN-beta)
Decreased peripheral conversion of T4 to T3
Decreased hypothalamic TRH secretion

Diagnostic testing

Early: Low T3, normal TSH & T4
Late: Low T3, TSH & T4

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7
Q

Congenital hypothyroidism

A

Usually asymptomatic at birth

After maternal thyroxine wanes (weeks to months)
Lethargy, poor feeding IMPORTANT
Enlarged fontanelle
Protruding tongue, puffy face, umbilical hernia
Constipation IMPORTANT
Prolonged jaundice
Dry skin

Delayed treatment is associated with neurocognitive dysfunction

Diagnosis
most commonly caused by abnormal thyroid gland development or location (ie, ectopy),
↑ TSH & ↓ free thyroxine levels
Newborn screening

IMPORTANT
thyroxine CROSS THE PLACENTA
TSH is a polypeptide hormone that does not cross the placenta.
Thyroglobulin does not cross the placenta

IMPORTANT:
Congenital goiter in the setting of hypothyroidism (ie, ↑ TSH, ↓ thyroxine) can be caused by transplacental passage of maternal antithyroid medications (eg, propylthiouracil PTU), which inhibit thyroid peroxidase and are used to treat maternal hyperthyroidism.

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8
Q

Central hypothyroidism

A

Causes

Mass lesions (eg, pituitary adenoma)
Pituitary surgery, trauma, irradiation
Infiltrative disorders (eg, sarcoidosis, hemochromatosis)
Pituitary infarction (eg, Sheehan syndrome) IMPORT

Clinical features

Hypothyroid symptoms
Mass-effect symptoms (eg, headache, visual field defects) if due to mass

Hormone levels

Low free thyroxine (T4)
Low or inappropriately normal TSH
Other pituitary hormone deficiencies (eg, ACTH, prolactin, gonadotropins)

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9
Q

Postpartum thyroiditis

A

IMPORTANT characterized by autoimmune destruction of thyroid follicles similar to that seen in chronic lymphocytic (Hashimoto) thyroiditis.
NON TENDER , LOW BLOOD FLOW

Pathophysiology

Autoimmune destruction of thyroid follicles & release of preformed thyroid hormone
Lymphocytic infiltrates ± germinal centers

Clinical course

Onset ≤12 months after pregnancy
Transient hyperthyroid phase (↑ T4 & T3, ↓ TSH)
Brief hypothyroid phase (↓ T4 & T3, ↑ TSH)
Return to euthyroid state

Diagnosis

↑ Serum thyroglobulin
↓ Radioiodine uptake
Ultrasonography: diffuse thyroid enlargement with ↓ blood flow

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10
Q

TBG

A

HIGH TBG IN PREGNANCY
HIGH total thyroxine (T4) and normal free T4 and TSH levels. Patients are euthyroid

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11
Q

Menopause

A

Menopause occurs on average at age 51 and is diagnosable retrospectively after 12 months of amenorrhea. An elevated serum FSH level confirms the diagnosis

FSH levels increase due to resistant ovarian follicles and lack of feedback from inhibin

Absence of menstrual cycles with associated hypoestrogenic symptoms (eg, hot flashes, vaginal dryness) is highly suggestive of menopause

Estradiol and progesterone levels gradually decrease during the menopausal transition due to decreasing ovarian function. Serum estradiol measurement is not a reliable indicator of menopause due to typical fluctuations and gradual decline. After menopause, estrone is produced outside the ovaries and replaces estradiol as the predominant circulating estrogen.

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12
Q

VIT D

A

Excessive vitamin D intake can lead to hypercalcemia and cause mental status changes, muscle weakness, constipation, and polyuria/polydipsia.

IMPORTANT
Activated macrophages in sarcoidosis and other granulomatous diseases express 1-α-hydroxylase, leading to excess production of 1,25-dihydroxyvitamin D and hypercalcemia.

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13
Q

INSULIN

A

Incretins are gastrointestinal hormones produced by the gut mucosa that stimulate pancreatic insulin secretion in response to sugar-containing meals. This response is independent of blood glucose levels, and typically occurs prior to any elevation in blood glucose level following a meal. Two hormones with incretin effects are glucagon-like peptide-1 (GLP-1) and gastric inhibitory peptide (glucose-dependent insulinotropic peptide, GIP). Insulin levels will also increase following intravenous administration of glucose due to the sensitivity of the pancreatic beta-cells to increases in blood glucose, but this increase will not be as marked as that seen following oral glucose administration because the effect of incretin is absent.

PROINSULIN STORED IN SECRETORY GRANULES
Endopeptidases in the secretory granules cleave proinsulin into insulin and C-peptide, which are then stored within the granules until they are secreted from the cell via exocytosis

LOW C-PEPTIDE LEVELS IN EXOGENOUS INSULIN

NO RELATION WITH LDL

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14
Q

Glucagon

A

Glucagon increases serum glucose by increasing hepatic glycogenolysis and gluconeogenesis. Glucagon also stimulates insulin secretion from the pancreas.
Unlike epinephrine, glucagon has an insignificant effect on glucose homeostasis in the skeletal muscle, adipose tissue, and renal cortex.

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15
Q

PROLACTIN

A

DOPAMIN INHIBIT BOTH TSH AND PROLACTINE

NOTE ALSO:
SOMATOSTATIN INHIBIT BOTH TSH AND GH

Hyperprolactinemia
SUPPRESION OF GnRH

Premenopausal women: Galactorrhea, estrogen deficiency (oligo/amenorrhea, decreased bone density, vaginal atrophy)
Men: Infertility, decreased libido, impotence
Children/adolescents: Delayed puberty, growth impairment

Mass-effect symptoms

Headache
Visual field defects
Suppression of other pituitary hormones

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16
Q

Brown adipose cells

A

Why newborns get cold easily

Brown adipose cells, which contain multiple lipid droplets and abundant mitochondria, produce large amounts of heat (ie, thermogenesis) by uncoupling oxidative phosphorylation with the protein thermogenin.

Preterm infants are at increased risk for hypothermia because they have less brown adipose tissue than term infants.

Newborn babies lose heat quickly because:

Their nervous system is immature → they can’t control body temperature well.

They have a large surface area compared to their body size → they lose heat faster.

They cannot shiver well → they can’t make heat by shivering like adults do.

Preterm (premature) babies have all these problems plus they have even less fat for heat production, so they get cold even more easily.

How newborns make heat: brown fat

Babies have a special type of fat called brown adipose tissue (brown fat).
It is found:

Above the collarbone

Around big blood vessels

Around organs in the abdomen

Brown fat helps keep babies warm without shivering.

Preterm babies have less brown fat → less heat production → more risk of hypothermia.

How brown fat works

Brown fat is different from regular (white) fat:

White fat: one big fat droplet

Brown fat: many tiny droplets + lots of mitochondria

The many mitochondria give brown fat its brown/tan color and allow it to produce heat.

Brown fat also has:

More oxygen use

More blood vessels
Because it is very active.

Special mechanism: thermogenin (UCP-1)

In most cells, mitochondria make ATP (energy).
But in brown fat, a protein called thermogenin (UCP-1) changes how mitochondria work.

Normally:

Protons flow back into the mitochondria → make ATP.

With thermogenin:

Protons leak back without making ATP.

The energy that would have made ATP is released as heat instead.

This process is called non-shivering thermogenesis.

17
Q

ADH

A

hypothalamic injury results in death of the magnocellular neurons, causing permanent central DI.

Damage to the more distal portions of the hypothalamic-hypophyseal tract (ie, below the infundibulum) (POST. PITUTARY)
typically causes transient DI because the cell bodies of the magnocellular neurons remain intact.

18
Q

post. pitutary

A

Vasopressin and oxytocin are synthesized and packaged with carrier proteins (neurophysins) within neurons found in the hypothalamus. The hormones are then transported down axonal projections to the posterior pituitary (neurohypophysis), where they are secreted into circulation.

19
Q

SIADH

A

is characterized by low plasma sodium and osmolality, inappropriately concentrated urine, and clinically normal volume status (euvolemic hyponatremia) IMPORTANT

The profound hyponatremia that occurs in SIADH can cause headache, weakness, altered mental status, and seizures.

20
Q

adrenal insufficiency

A

Suppression of the hypothalamus-pituitary-adrenal axis by glucocorticoid therapy is the most common cause of adrenal insufficiency

In these patients, adrenal crisis can be precipitated by stressful situations (eg, infections, surgery) if the glucocorticoid dose is not increased appropriately.
حتى لو بيوخذ جرعته المعتادة ما بتكفي

21
Q

cushing

A

In Cushing syndrome due to an ACTH-secreting pituitary adenoma (Cushing disease), ACTH is high and cortisol production can be suppressed by high-dose, but not low-dose, dexamethasone. In patients with ectopic ACTH production (eg, from malignant tumors), cortisol and ACTH production are not suppressed by low- or high-dose dexamethasone.

22
Q

DKA

A

Total body potassium deficit (LOSS IN URINE)

Despite the low intracellular potassium levels, extracellular potassium concentrations are normal or increased due to the following mechanisms:
1.Loss of intracellular free water caused by increased plasma osmolality leads to extracellular movement of potassium secondary to increasing intracellular potassium concentration
2.Lack of insulin also causes extracellular shifting of potassium

23
Q

PCOS

A

Polycystic ovary syndrome

Clinical features

1.Androgen excess: hirsutism, acne, androgenic alopecia
2.Ovarian dysfunction: menstrual irregularity, polycystic ovaries
3.Insulin resistance: acanthosis nigricans, glucose intolerance/diabetes, metabolic syndrome
Obesity

Treatment

1.Weight loss
2.Combination hormonal contraceptives
3.Metformin (if hyperglycemia/diabetes)

24
Q

SMALL TESTES

25
precocious puberty
ESTROGEN/TESTESTERON VS IGF ##Idiopathic precocious puberty is characterized by early-onset, pulsatile GnRH secretion, resulting in increased estrogen production. Estrogens promote bone growth but also epiphyseal plate (ie, growth plate) closure, so without treatment, patients typically have an early growth spurt but a shorter-than-expected adult height. A growth spurt occurs during early puberty primarily due to positive feedback by estrogen on growth hormone (GH) production. GH stimulates insulin-like growth factor 1 (IGF-1) synthesis, which leads to the differentiation and proliferation of chondrocytes in the epiphyseal plate and therefore increased linear growth
26
Functional hypothalamic amenorrhea
1.WIGH LOSS-- FAT LOSS 2.LEPTI PRODUCTION LOSS 3.GNRH REDUCED (BY HYPOTHULMUS) 4.FSH/LH REDUCED 5.ESTROGEN REDUCED ركز مهم كثير انه الاستروجين اخر اشي بنزل مش اول اشي results from loss of pulsatile GnRH release from the hypothalamus and is caused by weight loss, strenuous exercise, systemic illness, or abnormal eating habits. Loss of cyclic gonadotropin release leads to a decrease in LH and FSH secretion from the pituitary, which in turn causes low circulating estrogen levels.
27
hypopituitarism
Clinical features of hypopituitarism Etiology Pituitary causes Primary (eg, adenoma) or metastatic mass Infiltration (eg, hemochromatosis, lymphocytic hypophysitis) Hemorrhage (pituitary apoplexy) or infarction (Sheehan syndrome) POST DELIVARY Hypothalamic causes Mass lesions Radiation therapy Infiltration (sarcoidosis) Trauma to skull base Infections (tuberculosis meningitis) Clinical presentation ACTH deficiency (secondary adrenal insufficiency) Postural hypotension, tachycardia, fatigue, weight loss, hypoglycemia, eosinophilia Hypothyroidism (central) Fatigue, cold intolerance, constipation, dry skin, bradycardia, slowed deep-tendon reflexes Gonadotropins Women: amenorrhea, infertility Men: infertility, loss of libido ##Acute pituitary hemorrhage (pituitary apoplexy) is characterized by severe headache, bitemporal hemianopsia (compression of the optic chiasm), and ophthalmoplegia (compression of the oculomotor nerve [CN III]). It usually occurs in a preexisting pituitary adenoma. Pituitary apoplexy is a medical emergency that requires urgent treatment with glucocorticoids to prevent acute adrenal crisis and circulatory collapse.
28
HbA1c
##Use fructosamine instead ##Hemoglobin A1c (HbA1c) – Basics Formed by irreversible nonenzymatic glycosylation of hemoglobin (N-terminal) Reflects average blood glucose over ~3 months (RBC lifespan) ↑ Glucose or longer RBC exposure → ↑ HbA1c ##When HbA1c is FALSELY LOW ✅ Increased RBC turnover Beta-thalassemia minor ↑ HbA2 Microcytic RBCs → hemolysis ↓ RBC lifespan → falsely low HbA1c Use fructosamine instead ✅ Sickle cell disease / trait ↑ RBC destruction Trait: slight ↓ HbA1c Disease: marked ↓ HbA1c ✅ After treatment of: Iron deficiency Folate deficiency B12 deficiency → rapid release of young RBCs → ↓ HbA1c ##When HbA1c is FALSELY HIGH ✅ Decreased RBC turnover Untreated: Iron deficiency Folate deficiency Vitamin B12 deficiency → older RBCs persist → ↑ HbA1c ✅ Advanced diabetic nephropathy ↓ EPO production ↓ new RBCs → ↑ HbA1c TRUE High HbA1c ##Chronically elevated blood glucose (poor glycemic control) ##Key Alternative Test Fructosamine → reflects glycemia over 2–3 weeks Used when RBC lifespan is altered
29
hypoglycemia
confirmed by the Whipple triad: 1.Symptoms consistent with hypoglycemia (eg, tremor, diaphoresis, confusion) 2.Low blood glucose level 3.Relief of hypoglycemic symptoms when the blood glucose level is corrected C-PEPTIDE LEVELS TO KNOW IF ITS ENDO OR EXOGENOUS INSULIN
30
glucagonoma
Features of glucagonoma Clinical presentation 1.Necrolytic migratory erythema IMPORTANTTT Erythematous papules/plaques on face, perineum & extremities Lesions enlarge & coalesce, leaving a central indurated area with peripheral blistering & scaling 2.Diabetes mellitus/hyperglycemia 3.Gastrointestinal symptoms (diarrhea, anorexia, abdominal pain) Diagnosis Markedly elevated glucagon levels ##zinc deficiency can resemble necrolytic migratory erythema Zinc deficiency causes erythematous skin lesions (mainly around body orifices) that are predominantly vesicular and pustular. Other features (TO DEFERENTIATE) include hypogonadism, impaired taste and smell, night blindness, and impaired wound healing.
31
Pheochromocytoma
Pheochromocytoma is a malignancy arising from chromaffin cells of the adrenal medulla that typically presents with episodic headaches, diaphoresis, and hypertension. The adrenal medulla is derived from neural crest cells (multipotent, migratory cells that originate in ectoderm), which also give rise to melanocytes and neural ganglia. IMPORTANT ##NOTE: NORMALLY MEDULLA (Chromaffin cells are modified neuroendocrine cells derived from the neural crest) stimulated by acetylcholine
32
EMBRYO 1
The anterior pituitary is formed from an out-pouching of the pharyngeal roof and is called Rathke's pouch. The posterior pituitary gland arises from an extension of the hypothalamic neurons. ##Craniopharyngiomas are tumors arising from Rathke's pouch remnants in the anterior pituitary. They characteristically have three components: solid, cystic, and calcified. They present during childhood, usually, with mass effect and visual deficits.
33
EMBRYO 2
DiGeorge syndrome A 22q11.2 microdeletion results from maldevelopment of the third (inferior parathyroid and thymus) and fourth (superior parathyroid) pharyngeal/branchial pouches. Subsequent parathyroid and thymic hypoplasia results in hypocalcemia and T cell deficiency. Conotruncal cardiac anomalies (eg, interrupted aortic arch, truncus arteriosus) features such as hypertelorism, short palpebral fissures, micrognathia, bifid uvula, and cleft palate.
34
EBRYO 3
The thyroid gland is formed from an outpouching (evagination) of the pharyngeal epithelium and subsequently descends to the lower neck anterior to the upper trachea and larynx. The lowest part of the evagination forms the thyroid gland and the remaining portion forms the thyroglossal duct, which extends from the foramen cecum on the dorsal surface of the tongue to the superior border of the thyroid isthmus. IMPORTANT : Due to failure of migration, the thyroid can reside anywhere along the thyroglossal duct's usual path, including the tongue (lingual thyroid). Enlargement of a lingual thyroid can lead to obstructive symptoms (eg, dysphagia, dysphonia, dyspnea), typically during times of heightened thyroid stimulation (eg, puberty, pregnancy). Sometimes, this lingual thyroid is the only thyroid tissue in the body, so hypothyroidism can occur if it is removed.
35
ANATOMY
The superior thyroid artery and vein and external branch of the superior laryngeal nerve course together in a neurovascular triad that originates superior to the thyroid gland and lateral to the thyroid cartilage. The external branch is at risk of injury during thyroidectomy as it courses just deep to the superior thyroid artery. IMPORTANT : The cricothyroid muscle is the only muscle innervated by this nerve. The cricothyroid muscle acts to tense the vocal cords, and denervation injury may cause a low, hoarse voice with limited range of pitch. The internal branch of the superior laryngeal nerve does not innervate any muscles but provides sensory innervation to the laryngeal mucosa above the vocal folds. ##The remaining laryngeal muscles (Aryepiglotticus , Lateral cricoarytenoid ,Posterior cricoarytenoid, Thyroarytenoid) are innervated by the recurrent laryngeal nerves, which also provide sensory innervation to the larynx below the vocal folds. The recurrent laryngeal nerves lie posterior to the thyroid, near the inferior thyroid arteries. These nerves can be injured during thyroidectomy .