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Pathoma > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Pituitary Adenoma

A

Benign tumor anterior pituitary
functional if it secretes hormones, nonfunctional if it is silent
Nonfunctional tumors can present as mass effect (compress optic chiasm get bitemporal hemianopsia, compress ituitary = hypopituitarism, headache)

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2
Q

Prolactinoma

A

Pituitary Adenoma that secretes prolactin
galactorrhea and ammenorhea in females
decreased libido and headaches
Treat with dopamine agonists like bromocriptine or cabergoline

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3
Q

Growth Hormone Cell adenoma

A

Pituitary Adenoma that secretes GH
Children = gigantism
Adults = acromegally (large hands, feet, and jaw), growth of visceral organs leads to dysfunction (heart failure) and enlarged tongue
Also get secondary DM (GH decreases glucose uptake in cells)
Treat with ostreotide (somatostatin that supresses release of GH), GH Receptro antagonists, or surgery

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4
Q

ACTH Cell Adenomas

A

Pituitary Adenoma that secretes ACTH

Get Cushing Syndrome

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5
Q

Hypopituitarism

A

Insufficeint production of hormones by the anterior pituitary
Causes include
1) pituitary adenomas or craniopharyngioma with mass effects or pituitary apoplexy (bleeding into an adenoma)
2) Sheehan syndrome = pregnancy related infarction of the pituitary gland
3) Empty Sella Syndrome - herniation of the arachnoid and CSF into the sell compresses and destroys the pituitary gland

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6
Q

Sheehan Syndrome

A

Pituitary gland doubles in size during pregnancy but vasculature cannot keep up , blood loss during parturition precipitates infarction and leads to hypopituitarism

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7
Q

Hormones in Posterior Pituitary

A

ADH - acts on distal tubules and collecting ducts to promote free water retention
Oxytocin = mediates uterine contraction and release of breast milk
both are made in hypothalmaus and then transported to posterior by axonal transport

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8
Q

Central Diabetes Insipidus

A

ADH deficiency due to hypothalamic or posterior pituitary pathology
Get loss of free water leading to
1)polyuria and polydipsia with dangerous dehydration
2)hypernatremia and high serum osmolarity
Water deprivation test fails to increase urine osmolality
Treatment is desmopressin (ADH analog)

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9
Q

Nephrogenic Diabetes insipidus

A

Impaired renal response to ADH
Due to inherited mutations or drugs (lithium and demeclocycline)
Get loss of free water leading to
1)polyuria and polydipsia with dangerous dehydration
2)hypernatremia and high serum osmolarity
Does not respond to desmopressin treatment

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10
Q

Syndrome of Inappropriate ADH Secretion

A

Excessive ADH secretion
Usually due to ectopic production (small cell carcinoma of lung), CNS trauma, pulmonary infection, COPD, drugs like cyclophosphamide.
Retention of free water leads to
1) hyponatremia
2)Mental status change and seizures since hyponatremia leads to neuronal swelling and cerebral edema
treatment is free water restriction or democlocycline

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11
Q

Thyroglossal Duct Cyst

A

Cystic dilation of thyroglossal duct remnant which is supposed to normally involute.
Presents as an anterior neck mass

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12
Q

Lingual Thyroid

A

Persistence of thyroid tissue at the base of the tongue

Presents as a base of tongue mass

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13
Q

Mechanism and Symptoms of hyperthyroidism

A

Increased levels of circulating thyroid hormone 1) increases basal metabolic rate (by increasing synthesis of Na-K-ATPase) 2) Increases sympathetic nervous system activity (due to icnreased expression of Beta1 adrengergic receptors)
SYMPTOMS
weight loss, heat intolerance, tachycardia, arrythmia, tremor, anxiety, insomnia, diarrhea, oligomennorhea, bone resoprtion (hypercalcemia and osteoperosis), decreased muscle mass, HYPOCHOLESTEROLEMIA, HYPERGLYCEMIA

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14
Q

Grave Disease

  • mechanism
  • symptoms
  • Path
  • Labs
  • Treatment
  • Complications
A 
M = Autoantibody (IgG) that stimulates the TSH receptor (type II hypersensitivity) leads to increased synthesis and release of thyroid hormone.  Classically seen in women of childbearing age.
S = Get hyperthyroidism, diffuse goiter, exophthalmos and pretibial myxedema (fibroblasts behind the orbit and overlying the shin express the TSH receptor, activation results in GLYCOSAMINOGLYCAN buildup, inflammation, fibrosis, and edema)
P = irregular follicles with scalloped and chronic inflammation
L = Increased total and free T4, decreased TSH, hypocholesterolemia, increased serum glucose
T = Beta blockers, thioamide, and radioiodide ablation
C= Thyroid storm (elevated catecholamines and massive hormone excess, arrythmia, hyperthermia, and vomitting with hypovolemic shock) treat with propylthiouracil (inhibits peroxidase and peripheral conversion of T4 to T3), beta blockers, and steroids
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15
Q

Multinodular Goiter

A

Enlarged thyroid gland with multiple nodules
Due to relative iodine deficiency
Usually nontoxic
Rarely regions become TSH-independent leading to T4 release and hyperthyroidism (toxic goiter)

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16
Q

Cretinism

A

Hypothyroidism in neonates and infants
Characterized by mental retardation, short stature, caorse facial features, enlarged tongue, and umbilical hernia
Can be casued by maternal hypothyroidism in early pregnancy, thyroid agenesis, dyshormonogenetic goiter, and iodine deficiency (peroxidase mutation)

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17
Q

Myxedema

A

hypothyroidism in older children and adults
Clinical features based on decreased metabolic rate and decreased sympathetic nervous system activity
Get myxedema (results in DEEP VOICE and ENLARGED TONGUE), weight gain, slowing of mental activity, ,muscle weakness, cold intolerance, bradycardia, oligomenorrhea, HYPERCHOLESTEROLEMIA, constipation
Usually due to iodine deficiency, hashimoto thyroiditis, lithium, or surgical removal

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18
Q

Hasimoto Thyroiditis

A

Autoimmune destruction of thyroid gland, associated with HLA-DR5
Clinical presents intially as hyperthyroidism as preformed follicles release their T3, T4, but eventually progresses to hypothyroidism (decreased T4 and Increased TSH)
See Chronic inflammation with germinal centers and hurthle cells
Increased risk for B-Cell (marginal zone) lymphoma

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19
Q

Subacute Granulomatous (De Quervain) Thyroiditis

A

Granulomatous thyroiditis that follows a viral infection

Presents as tender thyroid with transient hyperthyroidisim. Usually self limited but may progress to hypothyroidism

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20
Q

Reidel Fibrosing Thyroiditis

A

Chronic Inflammation with extensive fibrosis of the thyroid gland
Hypothyroidism with a “HARD AS WOOD” nontender thyrid gland
Fibrosis may extend to involve local structures such as airways
See in YOUNG patients (40s)

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21
Q

“Hot” vs “Cold Nodule

A

I radioactive uptake studies are useful to charcteriz thyroid nodules.
Take up lots of I = hot = seen in graves disease or nodular goiter
Take up little I = cold = seen in adenoma and carcinoma, often warrants biopsy

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22
Q

How to biopsy Thyroid

A

Fine Needle Aspiration since it is highly vascualr and would bleed to much if do actual biopsy

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23
Q

Follicular Adenoma

A

Benign proliferation of follicles surrounded by a fibrous capsule.
Typically nonfunctional but can secrete thyroid hormone

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24
Q

Papillary Carcinoma

A

Most common thyroid carcinoma
Exposure to ionizing radiation in childhood is major risk factor
See papillae lined by cells with clear “orphan annie eye” nuclei and nuclear grooves, papillae are often associated with psammoma bodies
Often spreads to cervical lymph nodes

25
Q

Follicular Carcinoma

A

Malignant proliferation of follicles SURROUNDED by a fibrous capsule with INVASION through the capsule(unlike follicular adenoma)
Have to examine entire capsule not just a FNA
Mets HEMATOGENOUSLY (like chorio, renal, and hepatocellular carcinomas)

26
Q

Medullary Carcinoma

A

Malignant proliferation of parafollicular C cells
C Cells are neuroendocrine cells that secrete calcitonin which lowers serum calcium by increasing renal calcium excretion. Calcitonin can also deposit within a tumor as an amyloid
Biopsy reveals sheets of malignant cells in an amyloid stroma
Familial cases are often due Mutliple Endocrine Neoplasasia (MEN) 2A and 2B which are associated with mutations in RET oncogene
MEN 2 results in medullary carcinoma, pheochromocytoma, and parathyroid adenomas (2A) or ganglioneuromas of the oral mucose (2B)
RET mutation warrants prophylactic thyroidectomy

27
Q

MEN 2A and2B

A

Mutations in RET oncogene
MEN 2 results in medullary carcinoma, pheochromocytoma, and parathyroid adenomas (2A) or ganglioneuromas of the oral mucose (2B)
RET mutation warrants prophylactic thyroidectomy

28
Q

Anaplastic Carcinoma

A

Undifferentiated malignant tumor of the thyroid, usually seen in ELDERLY
Often invades local structures, leading to dysphagia or respiratory compromise
Poor prognosis

29
Q

Parathyroid Gland

A

Its Chief Cells regulate free ionzied calcium via PTH

1) Increases osteoclast activity (indirectly by activating osteoblasts) releasing calcium and phosphate
2) Increases small bowel absorption of calcium and phosphate (indirectly by activating vitamin D)
3) Increases renal calcium absoprtion (distal tubule) and decreases phosphate reabsorption (Proximal tubule)

30
Q

Primary Hyperparathyroidisim

Symptoms and labs

A

Excess PTH due to Parathyroid gland itself
Major cause is parathyroid adenoma but also sporadic parathyroid hyperplasia and parathyroid carcinoma
Usually asymptomatic hypercalcemia but can get
1) Nephrolithiasis
2) Nephrocalcinosis = metastatic calcification of renal tubules
3) CNS disturbance such as depression or seizures
4) Constipation, peptic ulcer disease, or Acute pancreatitis
Osteitis fibrosa cystica
Labs = Increased serum PTH, Ca2+, urincary cAMP, and serum alkaline phophatase, and decreased serum phosphate

31
Q

Secondary Hyperparathyroidisim

A

Excess Production of PTH due to disease extrinsic to parathyroid gland such as chronic renal failure
With chronic renal failure see decreased phosphate excretion which will increase serum phosphate that will bind calcium and therefore decrease serum free calcium. This will stimulate all 4 parathyroid glands to increase PTH to breakdown bone to increase calcium and lead to renal osteodystrophy
See increased PTH, serum phosphate, alkaline phosphate, and decreased serum calcium

32
Q

Hypoparathyroidisim

A

Low PTH. Causes include autoimmune damage, surgical excission or Digeorge syndrome (failure to develop parathyroid since 3rd and 4th pharyngeal pouch were missing)
Presents with low serum calcium that leads to numbness and tingling and muscle spasms that may be elicitied by filling up blood pressure cuff (trousseau sign) or tapping on the facial nerve (chvostek sign)
Labs show decreased PTH and serum calcium

33
Q

Troussea Sign

A

Muscle spasm upon filling up blood pressure cuff.

Can be sign of hypocalcemia due to hypoparathyrodisim

34
Q

Chvostek sign

A

Muscle spasm illicited by tapping on facial nerve

Can be sign of hypocalcemia due to hypoparathyrodisim

35
Q

Pseudohypoparathyrodisim

A

End organ resistance to PTH
Labs show hypocalcemia with increased PTH levels
Autosomal dominant form where GS is mutated and patients also are short in stature and have short 4th and 5th digits.

36
Q

Endocrine Pancreas

Cells and their functions

A

functional endocrine portion is the islets of langerhans
Beta cells lie in the center and secrete insulin which upregulates GLUT4 therefore increasing glucose uptake into cells and decreasing serum glucose
Alpha cells on the periphery secrete glucagon which increases serum glucose levels by stimulating glycogenolysis and lipolysis

37
Q

Type 1 Diaebtes Mellitus

A

Insulin deficiency leads to hyperglycemia
Results from autoimmune destruction of beta cells by T lymphocytes (type IV hypersensitivity). See inflammation of islets, HLA-DR3 and HLA-DR4, autoantibodies against insulin often present
Manifests in childhood with
1)High serum glucose
2)Weight loss, low muscle mass and polyphagia (eat a lot)
3) Polyuria, polydispsia, and glycosuria.
Treatment is lifetime replacement of insulin
High risk for DKA

38
Q

Diabetic Ketoacidosis

A

Condition seen in DM1.
Characterized by excessive ketones, often arises with stress such as infection where epinephrine levels are high and stiulate glucagon to exacerbate already high glucose levels.
There is increased lipolysis to increase free fatty acids that are converted to ketone bodies by the lvier.
See hyperglycemia (>300), anion gap metabolic acidosis, and hyperkalemia (that will be lsot in urine)
Present with Kussmaul respirations to breathe off acidosis, dehydration, nausea, vomiting, mental status changes, fruity breath
Treat with fluids, insulin, and replacement of electrolytes (potassium)

39
Q

Type 2 Diabetes Mellitus

A

End organ insulin resistance leading to metabolic disorder characterized by hyperglycemia
See in middle aged, obese (obesity decreases insulin receptors on cells), adults, with strong genetic predisposition
Insulin levels initially rise early in disease but beta cells become exhausted and insulin levels die down. See amyloid deposits in these islets.
Clinically silent but when do present they have polyuria, polydipsia, and hyperglycemia
Treat with weight loss, solfonylureas or metformin, or exogenous insulin.
Risk for hyper-osmolar non-ketoic coma = glucose above 500 leads to life threatening diuresis with hypotension and coma

40
Q

hyper-osmolar non-ketoic coma

A

Deadly complication of DM2

glucose above 500 leads to life threatening diuresis with hypotension and coma

41
Q

Long term consequences of Diabetes

A

Nonenzymatic glycosylation (NEG) of vascular basement membranes.

1) large and medium sized vessels = cardiovascular leads to death and peripheral vascular leads to need for amputations
2) small vessels = hyaline arterolosclerosis = renal arterioles leads to glomerulosclerosis with small scarred kidneys with a granular surface. Preferntial involvement of efferent arterioles leads to glomerular hyperfiltration with microalbuminuria that eventually progresses to nephrotic syndrome that is characterized by Kimmelstiel-Wilson Nodules

Osmotic Damage
Glucose freely enters schwann cells, pericytes of retinal blood vessels, and the lens
Aldose reductase converts glucose to soribtal, resulting is osmotic damage
Leads to peripheral neuropathy, impotence, blindness, and cataracts

42
Q

Tumors of Islet Cells

A

often a component of MEN1 along with parathyroid hyperplasia and pituitary adenomas

43
Q

Insulinomas

A

Episodic hypoglycemia with mental staus changes that are relieved by administration of glucose.
Diagnose by seeing decreased serum glucose, increased insulin, AND increased C-peptide

44
Q

Gastrinomas

A

Present as treatment resistant peptic ulcers (Zollinger-Ellison syndrome)

45
Q

Somatostatinomas

A

Achlorhydia (due to inhibition of gastrin) and cholelithiasis (gall stones) with steatorrhea (excess fat in feces) (both due to inhibition of cholecystokinin)

46
Q

VIPomas

A

Secrete excessive vasoactive intestinal peptide leading to watery diarrhea, hypokalemia, and achlorhydria (lack of gastric acid production)

47
Q

Layers of The Adrenal Cortex

A 
Glomerulosa = mineralcorticoids = aldosterone
Fasciculate = glucocorticoids = cortisol
Reticularis =sex steroids = testosterone
Kidney
"Sweeter as you go deeper"
"when thinking of kidney think of GFR"
48
Q

Symptoms and diagnosis of Hypercortisolism

A

Excess cortisol clinically presents as
1)muscle weakness with thin extremities
2) Moon facies, buffalo hump, and truncal obesity cus the high insulin increases storage of fat
3) Absominal striae from impaired synthesis of collagen
4) Hypertension
5) Osteoperosis
6) Immune Supression
Diagnose by increased 24hr urine cortisol levels

49
Q

Causes of Hypercortisolism

A

1) Exogenous corticosteroids = bilateral adrenal atrophy since steroids supress ACTH secretion
2) Primary adrenal adenoma, hyperplasia, or carcinoma = atrophy of uninvolved adrenal gland
3) ACTH-secreting pituitary adenoma = bilateral adrenal hyperplasia. High dose dexamethesaone supresses ACTH production by a pituitary adenoma and the cortisol levels derease
4) Paraneoplastic ACTH Secretion (small cell carcinoma of the lung) = bilateral adrenal hyperplasia = not responsive to high dose dexamethesaone and ACTH and cortisol levels remain high

50
Q

Hyperaldosteronism

-primary vs secondary

A

Excess aldosterone presents as hypertenion from sodium retention, hypokalemia, and metabolic alkalosis.
Primary = most commonly due to adrenal adenoma but also from spradic adrenal hyperplasia or adrenal carcnimoa. Characterized by high aldosterone and low renin
Secondary = seen in the activation of renin-angiotensin system (renovascular hypertension or CHE). See high aldosterone and high renin

51
Q

Congenital Adrenal Hyperplasia

A

Excess sex steroids with hyperplasia of both adrenal glands.
Inherited 21-hyroxylase deficiency is most common cause. It is required for production of aldosterone and cortisol so cholesterol shifts towards making all that it can now which is sex steroids. Lack of cortisol leads to increased ACTH scretion which causes the bilateral adrenal hyperplasia.
Clinically see Salt wasting with hyponatremia, hyperkalemia, and hypovolemia, life threatening hypotenison from lack of cortisol that activates alpha 1. See clitoral enlargmenet in women or precocious puberty in males

52
Q

Adrenal Insufficiency

A

Lack of adrenal hormones
Acute insufficiency may arise with Waterhouse-Friderichsen syndrome = hemmorhagic necrosis of the adrenal glands following DIC in young children with N meningitidis. The lack of cortisol exacerbates hypotension and leads to death
Chronic insufficiency = addison disease = progressive destruction of the adrenal glands by autimmune, TB, or metatastic carcinoma.
Clinically see hypotension, hyponatremia, hypovolemia, hyperkalemia, weakness, hyperpigmentation (especially in oral mucosa) vomitting and diarrhea

53
Q

Waterhouse-Friderichsen syndrome

A

adrenal insufficiency caused by hemmorhagic necrosis of the adrenal glands following DIC in young children with N meningitidis. The lack of cortisol exacerbates hypotension and leads to death

Clinically see hypotension, hyponatremia, hypovolemia, hyperkalemia, weakness, hyperpigmentation (especially in oral mucosa) vomitting and diarrhea

54
Q

addison disease

A

Chronic adrenal insufficiency from progressive destruction of the adrenal glands by autimmune, TB, or metatastic carcinoma.
Clinically see hypotension, hyponatremia, hypovolemia, hyperkalemia, weakness, hyperpigmentation (especially in oral mucosa) vomitting and diarrhea

55
Q

Pheochromocytoma

A

Tumor of chromaffin cells of the Adrenal Medulla.
Get increased serum catecholamines (epi and norepi) leads to episodic hypertenison, headache, palpitations, tachycardia, and sweating
Diagnose with increased serum metanephrins and increased 24hr urine metanephrines and vanillylmandelic acid.
Treat with surgical excision but first give them PHENOXYBENZAMINE (irreversible alpha blocker) to prevent a hypertensive crisis in middle of surgery
Rule of 10s = 10% bilateral, 10% familial, 10% malignant, 10% located outside of the adrenal medulla (bladder wall or organ of zuckerlandl)
Assoicated with MEN2A or MEN2B (RET mutations), Von-hippel-lindau, and neurofibromatosis type 1

56
Q

MEN 2A

A

RET mutation so Increased risk for
medullary carcinoma of thyroid
Pheochromocytoma
Parathyroid Adenoma

57
Q

MEN 2B

A

RET mutation so Increased risk of
medullary carcinoma of thyroid
Pheochromocytoma
Mucosal ganglioneuroma (especially in oral mucosa)

58
Q

von Hippel Lindau

A

Increased risk for
hemangioblastoma of the cerebellum
Renal cell carcinoma
Pheochromocytoma

Pathoma (25 decks)

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