Endocrine Pathology

1. Which type of goiter is expected in a patient with a TSH-secreting PITUITARY adenoma?

Cystic enlargement of the gland

*NODULAR/SMOOTH enlargement of the gland another weird cause of NODULAR/SMOOTH goiter is IODINE deficiency(TSH secretion increases in response to low Thyroxine),mechanism in both cases is hyperTROPHY of the gland.

Diffuse enlargement of the gland

Multinodular goiter with irregular borders

2. Toxic multinodular goiter causes diffuse vs nodular enlargement?

Fluctuating enlargement

*NODULAR enlargment.

Diffuse enlargement

Cystic enlargement

Toxic multinodular goiter typically presents with nodular enlargement rather than diffuse enlargement.

Explanation

Toxic multinodular goiter typically presents with nodular enlargement rather than diffuse enlargement.

3. Patient presents with symptoms of HYPOthyroidism, on history taking you note symptoms of HYPERthyroidism that followed 'Flu-like' infection, on examination thyroid is TENDER(SUPER HY), histology shows GRANULOMATOUS inflammation(Look for multinucleated giant cells), ESR is elevated. What is the likely diagnosis and prognosis?

*This is classic description of SUBacute granulomatous(de Quervan) thyrodITIS.it is HY to know that this thing is PAINFUL and is SELF-LIMITING with good prognosis(Goes away on its own)

The symptoms and findings suggest thyroid cancer, which may require surgical intervention and long-term management.

This could be indicative of Graves' disease, an autoimmune disorder leading to overactive thyroid.

This is likely a case of Hashimoto's thyroiditis, which is an autoimmune disorder causing chronic inflammation of the thyroid gland.

The correct diagnosis in this scenario is subacute granulomatous (de Quervan) thyroiditis, characterized by painful inflammation of the thyroid gland following a flu-like infection. This condition is self-limiting and has a good prognosis. Hashimoto's thyroiditis, Graves' disease, and thyroid cancer present with different clinical features and outcomes than what is described in the question.

Explanation

The correct diagnosis in this scenario is subacute granulomatous (de Quervan) thyroiditis, characterized by painful inflammation of the thyroid gland following a flu-like infection. This condition is self-limiting and has a good prognosis. Hashimoto's thyroiditis, Graves' disease, and thyroid cancer present with different clinical features and outcomes than what is described in the question.

4. MOST common symptom of Pituitary adenoma? HY anatomy correlate? MOST common type of pituitary adenoma?

The most common type of pituitary adenoma is Somatotroph adenoma

While Bitemporal hemianopia is often tested(As pituitary adenoma can compress optich chiasm), MOST common symptom is HEADACHE and it can be tested too.*MOST common pituitary adenoma is PROLACTINOMA(Derived from LACTOTROPHS-ACIDOPHILS)
*Second most common is NON-functioning tumors that present with signs of PANHYPOpituitarism(can even cause STOMACH pain,fatigue,excessive thirst/urination,basically any sign caused by decreased hormone levels of ANY Hormone from pituitary) along with signs of mass-effect(bitemporal hemianopsia,headache).*Somatotroph ademona secreting GH is third most common.

Pituitary adenoma most commonly presents with signs of hyperpituitarism

Bitemporal hemianopia is the most common symptom of Pitutary adenoma

5. Pituitary adenoma secreting GH increases risk of which cancers?diagnosis?What is Most common cause of death in these patients?Acromegaly vs Gigantism?

*Increased GH>Increased cell growth of proliferation>Increased risk of cancer(especially COLORECTAL Cancer/Polyps).*Most common cause of death in patients with pituitary tumor secreting GH is Heart failure(due to hyperTROPHY), hypertrophy in response to GH is also what contributes to LARYNGEAL/TONGUE swelling(Contributing to DEEPER voice) and development of colorectal polyps/cancer.*Gigantism is when GH secreting hormone affects persons BEFORE epiphysela plates close(>MORE LINEAR GROWTH>GIGANT) vs ACROMEGALY happens when epiphyesal plates have already closed(So you mainly increase width of bones usually HANDS and feet get larger/thicker and facial features become more coarse, especially MANDIBLE is affected>Separation of teeth on lower jow)..*GH has pulsatile secretion and thus isn't really used for diagnosis instead we use IGF1 levels(mediates effects of GH and is stable) but they might also hint you on GH secreting tumor if GH serum levels did NOT decrease in response to oral glucose(Normally hyperglycemia>Decreased GH secretion).MRI showing mass could also help(remember BODYBUILDER can be getting GH/IGF1 from exogenous sources for gains)*Treatment should BEGIN with SURGERY(remove adenoma), but they often test the fact that Long-acting Somatostatin analog(OCTREOTIDE) can be used for treatment and you should also know that growth hormone RECEPTOR antagonist known as PEGVISOMANT.*Dopamine AGONISTS(like carbergoline) can be used too.

Gigantism is when GH secreting hormone mainly affects bone density and structure.

Most common cause of death in patients with pituitary tumor secreting GH is respiratory failure.

Increased GH>Increased cell growth of proliferation>Increased risk of lung cancer.

6. A boy with dwarfism (Laron syndrome) presents with short stature, small head circumference, prominent forehead, saddle nose, and micropenis. Despite these physical characteristics, his growth hormone (GH) levels are increased. Why might his GH levels be increased?

Excessive consumption of GH supplements

Due to a pituitary tumor secreting excess GH

*He likely has dwarfism(laron syndrome) and thus his GH receptors can NOT be activated by GH, hence GH can't promote IGF1 from LIVER(HY)secretion to mediate its effects and so you get less feedback inhibition and so you get INCREASED serum GH with DECREASED IGF1.

Genetic mutation leading to GH hypersecretion

The boy's physical characteristics suggest dwarfism (Laron syndrome), which is characterized by GH insensitivity. Therefore, the incorrect answers proposing excess GH production, supplementation, or genetic mutation do not align with the underlying condition causing his increased GH levels.

Explanation

The boy's physical characteristics suggest dwarfism (Laron syndrome), which is characterized by GH insensitivity. Therefore, the incorrect answers proposing excess GH production, supplementation, or genetic mutation do not align with the underlying condition causing his increased GH levels.

7. Autosomal Dominant condition that causes LOSS of Function of G-protein coupled calcium receptors in parathyroid glands, what changes you expect in serum PTH, Calcium, Magnesium, and Urine calcium? How can you differ this condition from hyperparathyroidism?

LOSS of function of G-protein coupled calcium receptors in parathyroid glands leads to a decrease in PTH secretion, which does not have any significant impact on serum calcium or urine calcium levels.

LOSS of function of G-protein coupled calcium receptors in parathyroid glands causes an increase in PTH levels, resulting in a decrease in serum calcium levels and an increase in urine calcium levels.

*LOSS of function of G-protein coupled calcium receptors in parathyroid glands results in receptors that need to sense MORE calcium to suppress PTH secretion and thus those patients usually get Slight elevation of PTH that results in increased serum Calcium(HYPERcalcemia) by DECREASING calcium excretion(This also promotes reabsorbtion of magneseium>HYPERMagnesemia).In hyperparathyroidism URINE calcium usually increases because PTH increases overall load of calcium in the blood(i.e NET gain of calcium is so much that even though PTH decreases calcium excretion still the amount that was delivered to kidney and was filtered is greated than normal urine calcium levels) while here as elevation of PTH and calcium levels is mild, inhibitory effects of PTH on calcium excretion predominate>DECREASED urine calcium(+This is also contributed by Calcium sensing receptors in KIDNEY itself)

LOSS of function of G-protein coupled calcium receptors in parathyroid glands results in a decrease in PTH secretion, resulting in a decrease in serum calcium levels (HYPOcalcemia).

In the correct answer, the explanation provided clarifies how the loss of function of G-protein coupled calcium receptors affects serum PTH, Calcium, Magnesium, and Urine calcium levels in comparison to hyperparathyroidism. The incorrect answers present alternative scenarios that do not align with the described condition.

Explanation

In the correct answer, the explanation provided clarifies how the loss of function of G-protein coupled calcium receptors affects serum PTH, Calcium, Magnesium, and Urine calcium levels in comparison to hyperparathyroidism. The incorrect answers present alternative scenarios that do not align with the described condition.

8. Diabetes insipidus (either central or nephrogenic) causes a net loss of only water, leading to euvoemic hypernatremia. What changes would you expect in plasma osmolality/sodium levels, extracellular fluid (ECF) volume, and intracellular fluid (ICF) volume? How can this understanding help explain the use of thiazides for treatment, and what about indomethacin?

DI causes a net loss of both water and sodium, leading to hypovolemic hyponatremia.

Thiazide diuretics are used to promote retention of water and sodium in the body.

Plasma osmolality decreases due to an increase in total body water.

*DI causes NET loss of ONLY water(Just like FEVER does) leading to EUVOlemic HYPERnatremia(Volume is maintained by compensatory mechanisms controlling fluid depletion), POsm/Na increases because TBW decreases while TBNa stays the same, so as Na concentration increases in ECF which btw was contracted(You loose fluid in kidneys from ECF), water in ICF will move towards greater concentration of Na in ECF leading to contraction of ICF.*Because you don't really give a fuck so we give thiazide diuretics(+/-Amilorde) to promote volume loss(HYPERtonic loss of Na) so your body will increase reabsorption of Na/Water in PROXIMAL convoluted tubule, kinda same principle is utilized when we use NSAID-INDOMETHACIN as this guy will constrict afferent arteriole>Less perfusion>Your kidney will try to compensate by increased Proximal tubule reabsorbtion(Basically your kidney will try to hold on to every bit of water and Na and thus decrease the amount that is lost in urine).NOTE however that in CENTRAL DI preffered treatment is DESMOPRESSIN ACETATE(basically synthetic ADH) because here you just supplement what is missing and you are done.*Adequate hydration is CRUCIAL in both of those conditions.*ALSO Note if they ask about FIRST step in treatment of NEPHROGENIC DI look at stem if patient is on offending drug(Like LITHIUM for Bipolar disorder, first thing you should do is REMOVE the offending agent and substitute it with alternative)

The correct answer highlights the key concept of DI causing a net loss of only water, leading to hypernatremia. Thiazides are used to promote volume loss, while indomethacin can constrict the afferent arteriole to increase proximal tubule reabsorption.

Explanation

The correct answer highlights the key concept of DI causing a net loss of only water, leading to hypernatremia. Thiazides are used to promote volume loss, while indomethacin can constrict the afferent arteriole to increase proximal tubule reabsorption.

9. What type of hypertrophy is the most common cause of death in patients with GH-secreting adenoma?

Hyperplastic hypertrophy causing ARRHYTHMOGENIC cardiomyopathy

Symmetric hypertrophy causing RESTRICTIVE cardiomyopathy

*Eccentric hypertophy>DILATED cardiomyopathy.

Concentric hypertrophy causing HYPERTROPHIC cardiomyopathy

Patients with GH-secreting adenoma typically develop eccentric hypertrophy, leading to dilated cardiomyopathy, which can result in heart failure and increased mortality rates.

Explanation

Patients with GH-secreting adenoma typically develop eccentric hypertrophy, leading to dilated cardiomyopathy, which can result in heart failure and increased mortality rates.

10. How can you differentiate between psychogenic polydypsia and SIADH in a patient with decreased urine osmolarity?

Do water deprivation test, serum Na will decrease while urine osmolarity will increase in psychogenic polydypsia(Can be due to schyziphrenia) vs No real improvement with SIADH(Can be caused by CYCLOPHOSPHAMIDE,Head trauma,Small cell lung cancer)

Perform a blood glucose test to rule out diabetes insipidus, as it can mimic symptoms of both psychogenic polydypsia and SIADH

Order a brain CT scan to identify structural abnormalities in psychogenic polydypsia, while in SIADH focus on monitoring fluid intake

Administer vasopressin antagonist medication in both psychogenic polydypsia and SIADH to observe their response

11. What is the target of autoimmune destruction in adrenal gland, the most common cause of Addison disease (chronic primary adrenal insufficiency) in the Western world?

Target of destruction is insulin-producing beta cells in the pancreas.

*Target of destruction is CYTOCHROME P450 enzyme-21 hydroxylase.vsTB is most common cause of Addison disease in developing countries.

Target of destruction is vsTB (variable surface antigen Tuberculosis) in developing countries.

Target of destruction is thyroid peroxidase enzyme in the thyroid gland.

12. Which one of the following abnormalities is most closely associated with the woman's disorder?

C. Ectodermal dystrophy

When first it was described as primary adrenal insufficiency, the most common cause was tuberculosis of the adrenal gland. Now the majority of patients have adrenal autoantibodies and are thought to have autoimmune Addison’s disease. Autoimmune adrenalitis may occur by itself (isolated autoimmune Addison’s disease) or it may occur with other autoimmune endocrine diseases. Two major patterns of autoimmune polyendocrine syndromes have been described. In addition to autoimmune adrenitis, patients with autoimmune polyendocrine syndrome type (APS1) have chronic mucocutaneous candidiasis and abnormalities of the skin, nails, and teeth (ectodermal dystrophy). APS1 is also known as APECED (autoimmune polyendocrinopathy, candidiasis, and Ectodermal dystrophy). In addition patients have other autoimmune disorders including autoimmune hypoparathyroidism, idiopathic hypogonadism, and pernicious anemia. APS1 result from mutations of the autoimmune regulator (AIRE) gene, the product of which is expressed primarily in the thymus.

Autoimmune polyendocrine syndromes type 2 (APS2) is not associated with candidiasis, ectodermal dysplasia, or autoimmune hypoparathyroidism.
Instead, autoimmune adrenalitis is present with autoimmune thyroiditis (Hashimoto’s thyroiditis) or type 1 diabetes mellitus.

D. Parathyroid hyperplasia

B. Diabetes mellitus

When first described as primary adrenal insufficiency, the most common cause was tuberculosis of the adrenal gland. Now the majority of patients have adrenal autoantibodies and are thought to have autoimmune Addison's disease. Autoimmune adrenalitis may occur with other autoimmune endocrine diseases. Two major patterns of autoimmune polyendocrine syndromes have been described. In addition to autoimmune adrenitis, patients with autoimmune polyendocrine syndrome type (APS1) have chronic mucocutaneous candidiasis and abnormalities of the skin, nails, and teeth (ectodermal dystrophy). APS1 is also known as APECED (autoimmune polyendocrinopathy, candidiasis, and Ectodermal dystrophy). In addition patients have other autoimmune disorders including autoimmune hypoparathyroidism, idiopathic hypogonadism, and pernicious anemia. APS1 result from mutations of the autoimmune regulator (AIRE) gene, the product of which is expressed primarily in the thymus.Autoimmune polyendocrine syndromes type 2 (APS2) is not associated with candidiasis, ectodermal dysplasia, or autoimmune hypoparathyroidism.Instead, autoimmune adrenalitis is present with autoimmune thyroiditis (Hashimoto's thyroiditis) or type 1 diabetes mellitus.

Explanation

When first described as primary adrenal insufficiency, the most common cause was tuberculosis of the adrenal gland. Now the majority of patients have adrenal autoantibodies and are thought to have autoimmune Addison's disease. Autoimmune adrenalitis may occur with other autoimmune endocrine diseases. Two major patterns of autoimmune polyendocrine syndromes have been described. In addition to autoimmune adrenitis, patients with autoimmune polyendocrine syndrome type (APS1) have chronic mucocutaneous candidiasis and abnormalities of the skin, nails, and teeth (ectodermal dystrophy). APS1 is also known as APECED (autoimmune polyendocrinopathy, candidiasis, and Ectodermal dystrophy). In addition patients have other autoimmune disorders including autoimmune hypoparathyroidism, idiopathic hypogonadism, and pernicious anemia. APS1 result from mutations of the autoimmune regulator (AIRE) gene, the product of which is expressed primarily in the thymus.Autoimmune polyendocrine syndromes type 2 (APS2) is not associated with candidiasis, ectodermal dysplasia, or autoimmune hypoparathyroidism.Instead, autoimmune adrenalitis is present with autoimmune thyroiditis (Hashimoto's thyroiditis) or type 1 diabetes mellitus.

13. Why is HYPERpigmentation extremely characteristic of Addison's disease?

Because it is a common symptom in all types of adrenal insufficiency.

*Because it ties with physiology(POMC breaks into MSH and ACTH , thus when we increase synthesis of ACTH from POMC we also increase MSH which stimulates melanin production), also HYPERpigmentation is ONLY characteristic for PRIMARY adrenal insufficiency(In secondary and tertiary ACTH levels are actually DOWN not up).*Very HY to know,they develop HYPERkalemic metabolic acidosis(Lack of aldosterone>Less H and K excreted)

Because it is a side effect of the electrolyte imbalances caused by Addison's disease.

Because patients with Addison's disease have higher levels of cortisol, which leads to increased melanin production.

The correct answer explains the physiological relationship between ACTH, MSH, and melanin production in Addison's disease, as well as the specific association with primary adrenal insufficiency. It also mentions the development of HYPERkalemic metabolic acidosis in these patients due to aldosterone deficiency.

Explanation

The correct answer explains the physiological relationship between ACTH, MSH, and melanin production in Addison's disease, as well as the specific association with primary adrenal insufficiency. It also mentions the development of HYPERkalemic metabolic acidosis in these patients due to aldosterone deficiency.

14. Addisonian crisis(LIFE-THREATENING condition that can manifest with severe hypoglycemia,Hypotension,fever,convulsions,coma) is primarily mediated by lack of which hormone?

Aldosterone

Thyroxine

*CORTISOL(choose this over aldosterone which is deficient in this case too but acute lack of cortisol is what leads to this life-threatening acute condition).CLASSIC case they love is MENINGOCOCCEMIA(Like N.meningitis infects college student who now presents with neck stiffness and Deep purple NON-blanchable rash)>HEMORRHAGE into adrenal glands>ACUTE primary adrenal insufficiency.(<No hyperpigmentation because it usually kills you before you have chance to increase synthesis of melanin enough)*STRESS can precipitate this condition in patients with PRIMARY CHRONIC adrenal insufficiency(Addison disease) because stress increases demand on cortisol.

Insulin

In cases of Addisonian crisis, the lack of cortisol plays a primary role in the life-threatening condition. While aldosterone deficiency is also present in this scenario, the acute lack of cortisol is the main cause. Insulin and thyroxine are not directly related to Addisonian crisis.

Explanation

In cases of Addisonian crisis, the lack of cortisol plays a primary role in the life-threatening condition. While aldosterone deficiency is also present in this scenario, the acute lack of cortisol is the main cause. Insulin and thyroxine are not directly related to Addisonian crisis.

15. What are the results of a Metyrapone test in Addison's disease?

In Addison's disease, a Metyrapone test will show normal cortisol, ACTH, and 11 deoxycortisol levels.

In Addison's disease, a Metyrapone test will show decreased ACTH levels.

In Addison's disease, a Metyrapone test will show increased cortisol levels.

*Whenever you have PRIMARY adrenal insufficiency, metyrapone test(11 B hydroxylase inhibitor that blocks turning of 11DeOxyCortisol into cortisol), ACTH will increase even more but 11 deoxycortisol levels still remain low(Because problem is in your adrenal gland cells)cortisol levels will decrease even more, contrast this with increased 11deoxycortisol+LOW ACTH levels,coupled with decreased cortsiol with metyrapone stimulation test in patient with secondary adrenal insufficiency.

In primary adrenal insufficiency like Addison's disease, the Metyrapone test results in increased ACTH levels due to the lack of negative feedback from cortisol, leading to decreased cortisol levels and low 11 deoxycortisol levels. This is characteristic of a dysfunction in the adrenal gland cells.

Explanation

In primary adrenal insufficiency like Addison's disease, the Metyrapone test results in increased ACTH levels due to the lack of negative feedback from cortisol, leading to decreased cortisol levels and low 11 deoxycortisol levels. This is characteristic of a dysfunction in the adrenal gland cells.

16. Do you expect to see hyperkalemic metabolic acidosis in patient with Addison disease vs Adrenal insufficiency secondary to pituitary apoplexy? what about hyperpigmentation?

In Addison disease, hyperkalemic metabolic acidosis is not typically present, and hyperpigmentation is minimal due to the partial destruction of adrenal cells.

In adrenal insufficiency secondary to pituitary apoplexy, hyperkalemic metabolic acidosis is commonly observed, along with hyperpigmentation as a result of the pituitary dysfunction impacting aldosterone levels.

In Addison disease, hyperkalemic metabolic acidosis is typically seen due to the dysfunction of the adrenal glands, while hyperpigmentation may or may not be present depending on the severity of the disease.

*In addison disease you would expect to see that because CELLS of adrenal gland are killed and thus cells that secrete aldosterone are killed too(>Less H and K excretion)vsIn SECONDARY causes you don't see those abnormalities because zona glomerulosa does NOT need ACTH to produce aldosterone(It needs Angiotensin2), so even though your cortisol is low, your aldosterone is fine and you don't usually develop hyperkalemic metabolic acidosis.*Remember LOW ACTH levels is the problem in secondary(hence no hyperpigmentation)vs*Dead adrenal is problem in primary(>leading to compensatory increase in ACTH>HYPERpigmentation)

17. Patient develops signs of adrenal failure after acute removal of corticosteroids, will he have HYPERkalemia?

*NO because problem here is supression of ACTH secretion by providing too much steroids, then acute withdrawal doesn't give time to your adrenals to re-adjust>adrenal failure, BUT Aldosterone secretion is not dependent on ACTH so it needs no adjustments and thus K levels will be fine.

No, because adrenal failure always results in hyperkalemia regardless of the cause.

Yes, because acute removal of corticosteroids disrupts normal potassium levels in the body.

Yes, because adrenal failure leads to excessive production of aldosterone causing hyperkalemia.

The correct answer explains that hyperkalemia is not expected in this scenario due to the specific relationship between corticosteroids, ACTH, and aldosterone levels.

Explanation

The correct answer explains that hyperkalemia is not expected in this scenario due to the specific relationship between corticosteroids, ACTH, and aldosterone levels.

18. Why would you get EUVOLEMIC(Normal volume) HYPOnatremia in SIADH?significance of HYPOnatremia?

A. Hypernatremia because of excessive salt intake.

C. Hypervolemia leading to increased sodium levels in the blood.

*HYPONatremia because you gain PURE water and no salt.EUVOLEMIC because even though you gain fluids by free water you also loose proportional amount because your body will try to comepnsate by decreasing aldosterone and increasing ANP and BNP(all leading to dumping of Na into urine, which decreases serum Na even more but guess what some of that extra fluid you got from all that ADH will follow that Na too and so you maintain normal volume),increased ANP,BNP,decreased aldosterone>NORMAL ECF VOLUME is answer for question where they ask for mechanism of NO edema in patient with SIADH.HYPOnatremia=Less salt in ECF>Water will leave ECF and follow more salt In ICF>Cerebral edema and Seizures(often tested).their FAV. question though is description of Hyponatremia and then rapid correction and suddenly patient developing quadriplegia and asking what happened and answer is OSMOTIC demyelination secondary to rapid correction of HYPOnatremia.

B. Hypokalemia due to potassium loss in the urine.

The correct answer explains the mechanism of EUVOLEMIC HYPOnatremia in SIADH. Option A is incorrect as it mentions hypernatremia which is the opposite of the scenario described. Option B is incorrect as it refers to hypokalemia which is not directly related to the condition. Option C is incorrect as it discusses hypervolemia which is not characteristic of SIADH-induced HYPOnatremia.

Explanation

The correct answer explains the mechanism of EUVOLEMIC HYPOnatremia in SIADH. Option A is incorrect as it mentions hypernatremia which is the opposite of the scenario described. Option B is incorrect as it refers to hypokalemia which is not directly related to the condition. Option C is incorrect as it discusses hypervolemia which is not characteristic of SIADH-induced HYPOnatremia.

19. What is the most common cause of HYPOpituitarism in adults and children?

*Even though most common pituitary adenoma is prolacitnoma, most common cause of HYPOPituitarism is acutally NON-functioning adenoma.(Prolacitnoma gets treated before it has chance to lead to hypopituitarism as it has other manifestations like galactorrhea, but non-functioning adenoma has time to grow as it is initially asymptomatic and when it becomes massive it compresses other parts of pituitary leading to hypopituitarism)NOW in children most common cause of Hypopituitarism is CRANIOPHARYNGIOMA(Remnant of rathke's pouch that grows in SUPRAsellar region)

Adrenocorticotropinoma

Somatotropinoma

Prolactinoma

Prolactinoma can lead to symptoms like galactorrhea before causing hypopituitarism. Somatotropinoma and Adrenocorticotropinoma are less common causes compared to NON-functioning adenoma in adults.

Explanation

Prolactinoma can lead to symptoms like galactorrhea before causing hypopituitarism. Somatotropinoma and Adrenocorticotropinoma are less common causes compared to NON-functioning adenoma in adults.

20. Why might a patient who gave birth to a child recently (cesarean section) present with intolerance to cold, amenorrhea, and inability to breastfeed her child?

*SIgns of hypopituitarism in woman with recent pregnancy=SHEEHAN syndrome(VERY HY to know that it is due to ISCHEMIC INFARCT of Pituitary gland-COAGULATIVE necrosis, because it is NOT part of brain<SUPER HY)This happens because with pregnancy vascularization and size of pituitary increases but after delivery(BLOOD LOSS)>HYPOPerfusion of this big o pituitary>COAGULATION necrosis.Another HY thing to know about this condition is that they get sudden onset of LOSS of PUBIC HAIR.

Postpartum depression leading to hormonal imbalance

Side effects of medications given during the cesarean section

Autoimmune thyroiditis causing thyroid dysfunction

Sheehan syndrome is a rare condition that occurs due to vascular insufficiency post-delivery, leading to ischemic infarct of the pituitary gland. This results in hormonal imbalances affecting various functions such as intolerance to cold, amenorrhea, and inability to breastfeed. The incorrect answers do not match the specific mechanism and presentation of Sheehan syndrome.

Explanation

Sheehan syndrome is a rare condition that occurs due to vascular insufficiency post-delivery, leading to ischemic infarct of the pituitary gland. This results in hormonal imbalances affecting various functions such as intolerance to cold, amenorrhea, and inability to breastfeed. The incorrect answers do not match the specific mechanism and presentation of Sheehan syndrome.

21. What condition presents with sudden onset of severe headache, photophobia, nuchal rigidity, ocular symptoms like diplopia and bitemporal hemianopsia, and hypotension due to adrenal insufficiency?

Subarachnoid hemorrhage, which can lead to sudden severe headache, photophobia, and nuchal rigidity due to bleeding into the subarachnoid space

Meningitis characterized by inflammation of the meninges and typically presents with severe headaches and nuchal rigidity

Acute angle-closure glaucoma presenting with sudden severe eye pain, blurred vision, and halos around lights

*This is classic for Pituitary aproplexy which is basically sudden hemorrhage into pituitary usually due to existing pituitary adenoma,pituitary aproplexy>Hypopituitarism(especially secondary AI).*Because hemorrhage expands in the region of sella turcica cranial nerves that pass trough cavernous sinus(III,IV,V1,2,VI,) can be compressed>Palsies, bitemporal hemianopsia is also possibility due to optic chiasm compression(Cranial nerve 2=optic nerve).GLUCOcorticoids should be supplemented ASAP(lack of ACTH>lack of glucocorticoids>Addisonian crisis which can KILL you), other hormone replacement therapies might also be needed(like thyroxin, due to lack of TSH from anterior pituitary)

22. What is the first step in the treatment of a patient who develops HYPOPituitarism due to a NON-functional adenoma?

Wait for spontaneous regression of the adenoma

*FIRST try HORMONE REPLACEMENT THERAPY(For whatever is deficienty, like THYROXINE,GH,Corticosteroids,Sex hormones)then remove the mass if necessary.

Start chemotherapy for the patient

Perform immediate surgery to remove the adenoma

The correct first step in the treatment of a patient with HYPOPituitarism due to a NON-functional adenoma is to try HORMONE REPLACEMENT THERAPY before considering surgical removal of the mass, as it helps restore hormone levels and function.

Explanation

The correct first step in the treatment of a patient with HYPOPituitarism due to a NON-functional adenoma is to try HORMONE REPLACEMENT THERAPY before considering surgical removal of the mass, as it helps restore hormone levels and function.

23. If a patient presents with PROXIMAL muscle weakness, what can be inferred about their CK levels and symptoms based on thyroid function?

PROXIMAL muscle weakness is not related to thyroid function, thus CK levels will remain normal and the patient will present with chest pain as a symptom.

*PROXIMAL muscle weakness is classic for thyroid problems and most importantly HYPOthyroidism>INCREASED CK levels(Marker of MYOCYTE DEATH)vs HYPERthyrodism>NORMAL CK levels.HYPOthyroidism is also characterized by DYSPNEA on exertion vs HYPERthyroidism causes atrial fibrilation(Due to INCREASED Number of B receptors and their increased Sensitivity to catecholamines)

PROXIMAL muscle weakness is indicative of a heart condition, which may lead to INCREASED CK levels and DYSPNEA on exertion as symptoms, regardless of thyroid function.

PROXIMAL muscle weakness is classic for HYPERthyroidism, which is likely to have NORMAL CK levels and present with atrial fibrillation as a symptom.

Proximal muscle weakness is a key indicator of thyroid dysfunction, with HYPOthyroidism being associated with increased CK levels and dyspnea on exertion. It is important to differentiate between hypo- and hyperthyroidism based on CK levels and symptoms to provide appropriate treatment.

Explanation

Proximal muscle weakness is a key indicator of thyroid dysfunction, with HYPOthyroidism being associated with increased CK levels and dyspnea on exertion. It is important to differentiate between hypo- and hyperthyroidism based on CK levels and symptoms to provide appropriate treatment.

24. What is the difference between pretibial myxedema and myxedema anywhere else?

Addison's disease commonly presents with myxedema anywhere else on the body due to adrenal insufficiency.

Hashimoto's thyroiditis is characterized by exophthalmos and myxedema anywhere else on the skin as a result of autoimmune destruction of the thyroid gland.

*GRAVES disease is characterized by EXOPTHALMOS and PRETIBIAL MYXEDEMA(MECHANISM:Increased fibroblast response and mucopolysaccharide deposition in DERMIS of skin in response to AUTOANTIBODIES)vsMyxedema anywhere else should make you think of HYPOthyroidism.

Cushing's syndrome is associated with pretibial myxedema and presents with hyperpigmentation on the skin.