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Most common cause of exogenous Cushing syndrome
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Section 1
(50 cards)
Most common cause of exogenous Cushing syndrome
Exogenous corticosteroids
Neuroendocrine tumors originate from which two types of cells?
1. Kulchitsky cells 2. Enterochromaffin-like cells
Metyrapone stimulation test results: Secondary/tertiary adrenal insufficiency
Decreased ACTH Decreased 11-deoxycortisol
Increased ACTH What's the next step?
ACTH-dependent Cushing Syndrome Next step: Distinguish between Cushing Disease and Ectopic ACTH secretion with High dose dexamethasone suppression test and CRH stimulation test
Causes of primary hyperaldosteronism
Adrenal adenoma (Conn Syndrome) Idiopathic adrenal hyperplasia
Aldosterone/renin in secondary hyperaldosteronism
Increased aldosterone Increased renin
In secondary hyperaldosteronism, why is there increased renin?
Independent activation of RAAS due to Juxtaglomerular cell tumor Renovascular hypertension
Metyrapone stimulation test results for: Primary adrenal insufficiency
Increased ACTH Decreased 11-deoxycortisol
What is the most common cause of Addison Disease in the developing world?
TB
Patient presentation: Abdominal distension Firm, irregular mass that can cross midline Opsoclonus-myoclonus syndrome (dancing eyes-dancing feet) Labs: Increased HVA and VMA in urine (Catecholamine metabolites) homer-Wright rosettes Bombesin and NSE positive Overxpression of N-myc oncogene
Neuroblastoma APUD tumor
Metyrapone stimulation test Tests for primary/secondary/tertiary adrenal insufficiency
Blocks metyrapone step of cortisol synthesis: 11-deoxycortisol-->cortisol Normal response: decreased cortisol with compensatory increased ACTH
Decreased ACTH with high dose dexamethasone suppression test
Cushing Disease
Increased ACTH and cortisol with CRH suppression test (Prior increased measured ACTH)
Cushing disease
Secondary hyperaldosteronism is seen in patients with what?
Renovascular hypertension Juxtaglomerular cell tumor (independent activation of RAAS)
Neuroendocrine tumor in adrenals
Pheochromocytoma
Cushing Syndrome
Increased cortisol
This is associated with autoimmune polyglandular syndromes A. Primary adrenal insufficiency B. Secondary " C. Tertiary "
Primary adrenal insufficiency
What is the most common cause of Addison Disease in the Western World?
Autoimmune destruction
ACTH/cortisol in secondary/tertiary adrenal insufficiency
Low cortisol Low ACTH
Neuroendocrine tumors contain what?
Precursor uptake decarboxylase (APUD), secreting different hormones
Where do neuroblastomas occur?
Anywhere along the sympathetic chain
Waterhouse-Friderichsen Syndrome
Acute primary adrenal insufficiency due to Adrenal hemorrhage associated with septicemia: Neisseria meningitidis DIC Endotoxic shock
Cushing syndrome etiology
Increased cortisol: 1. Exogenous corticosteroids (bilateral adrenal atrophy) 2. primary adrenal adenoma, hyperplasia, carcinoma. Atrophy of uninvolved gland. 3. ACTH-secreting pituitary adenoma (Cushing disease). Paraneoplastic ACTH secretion. Results in bilateral adrenal hyperplasia.
Neuroblastomas originate from what type of cells?
Neural crest cells
Symptoms of Cushing syndrome
Hypertension Weight gain Moon facies Abdominal striae Truncal obesity Buffalo hump Skin changes (thinning, striae) Osteoporosis Hyperglycemia Amenorrhea Immunosuppression
Causes of Increased ACTH
Cushing disease (ACTH-secreting pituitary adenoma)
Inability of adrenal glands to generate enough glucocorticoids
Adrenal insufficiency
In secondary and tertiary adrenal insufficiency, is aldosterone synthesis preserved
Yes! No hyperkalemia.
Most common adrenal medulla tumor in children <4 years old
Neuroblastoma
Primary adrenal insufficiency
Deficiency of aldosterone AND Cortisol production: Hypotension (hyponatremic volume contraction) Hyperkalemia Metabolic acidosis Skin + mucosal hyper pigmentation
Increased ACTH with high dose dexamethasone suppression test
Ectopic ACTH suppression
ACTH/cortisol in primary adrenal insufficiency
Low cortisol High ACTH
In hyperaldosteronism, is there edema? Why?
No! Aldosterone escape mechanism
Neuroendocrine tumor in prancreas
Islet cell tumor
Primary/Secondary/Tertiary adrenal insufficiency: Decreased pituitary ACTH production No skin/mucosal hyper pigmentation No hyperkalemia
Secondary adrenal insufficiency Secondary Spares the skin/mucosa
Neuroendocrine tumor in thyroid
Medullary carcinoma
Chronic Primary adrenal insufficiency (Addison Disease
Adrenal atrophy or destruction
What are the causes of decreased ACTH?
Exogenous glucocorticoids Adrenal tumor
Decreased ACTH Causes
ACTH-independent cushing syndrome Caused by: - Exogeneous glucocorticoids - Adrenal tumor
No increase in ACTH and cortisol with CRH suppression test (Prior increased measured ACTH)
Ectopic ACTH secretion
Most common cause of endogenous Cushing syndrome
Cushing disease (ACTH-secreting pituitary adenoma)
Hyperaldosteronism: Metabolic alkalosis Metabolic acidosis
Metabolic alkalosis
Neuroendocrine tumor in lungs
Small cell carcinoma
Primary/Secondary/Tertiary adrenal insufficiency: Seen in patients with chronic exogenous steroid use--precipitated by abrupt withdrawal. Unaffected aldosterone synthesis
Tertiary Tertiary from Treatment
Treatment of Adrenal insufficiency
Glucocorticoid or mineralocorticoid replacement
Symptoms of adrenal insufficiency
Weakness Fatigue Orthostatic hypotension Muscle aches Weight loss GI disturbances Sugar/salt cravings
Cushing Disease
ACTH-secreting pituitary adenoma)
Hypertension Normal or hypokalemia Metabolic alkalosis
Hyperaldosteronism NO edema - due to aldosterone escape mechanism
Screening tests for Cushing syndrome
1. Increased free cortisol on 24 hour urinalysis 2. Increased midnight salivary cortisol 2. No suppression with overnight low-dose dexamethasone test
Acute primary adrenal insufficiency
Sudden onset (massive hemorrhage) Can present with SHOCK in a adrenal crisis
Section 2
(50 cards)
What medications can cause hypothyroidism?
Amiodarone Lithium
Associated with increased risk of non-Hodgkin lymphoma (B-cell origin)
Hashimoto thyroidits
Pheochromocytoma secrete what?
Epinephrine Norepinephrine Dopamine Increased catecholamines + metanephrines in urine and plasma
Pathophysiology of Exophthalmos in Graves Disease
1. Activated T-cells infiltrate rtetroorbital space, increasing cytokines (TNF-alpha, IFN-gamma) 2. Which increases fibroblast secretion of hydrophilic GAGs 3. Which increases osmotic muscle swelling, muscle inflammation, and adipocyte count 4. EXOPHTHALMOS Presents during stress (pregnancy)
Thyroid peroxidase
1. Catalyzes oxidation of Iodide --> Iodine 2. Iodination of thyroglobulin 3. Couples run between 2 iodized tyrosine residues
Increased catecholamine metabolites (HVA and VMA)
Neuroblastoma
Riedel thyroiditis
Thyroid replaced by fibrous tissue with inflammatory infiltrate Can extend to local structures Manifestation of IgG4-related systemic disease Fixed, hard (rock-like), PAINLESS goiter
Why is there pretibial myxedema in Graves Disease?
Thyroid stimulating immunoglobulin (IgG) stimulates TSH receptors on dermal fibroblasts.
Moderately enlarged, nontender thyroid
Hashimoto thyroiditis
Inflammation found in subacute granulomatous thyroiditis (de Quervain)
Granulomatous inflammation
True or false: Hashimoto thyroiditis can be hyperthyroid early on.
True. Why?: Thyrotoxicosis during follicular rupture
Pheochromocytoma, rule of 10s
10% malignant 10% bilateral 10% extra-adrenal 10% calcify 10% kids
Type of hyperthyroidism that presents with: Delirium Fever Diarrhea Coma Tachyarrythmia May present with increased LFTs
Thyroid storm
Hypothyroidism or hyperthyroidism? Increased creatine kinase
Hypothyroidism
In hyperthyroidism, what is the cause of chest pain, palpitations and arrhythmias?
Increased # and sensitivity of beta-adrenergic receptors
Hyperthyroidism or hypothyroidism: Warm, moist skin Fine hair Normal CK
Hyperthyroidism
Pheochromocytoma derived from what cells?
Chromatin cells (from neural crest) Some from gremline mutations too
Thyroid replaced by fibrous tissue with inflammatory infiltrate Can extend to local structures Manifestation of IgG4-related systemic disease Fixed, hard (rock-like), PAINLESS goiter
Riedel thyroiditis
Wolff-Chiakoff effect
Thyroid gland downregulation in response to increased iodide
What type of hypersensitivity response is Graves Disease?
Type II hypersensitivity
Most common tumor of the adrenal medulla in adults
Pheochromocytoma
Causes of smooth/diffuse goiter
1. Graves disease 2. Hashimoto thyroiditis 3. Iodine insufficiency 4. TSH-secreting pituitary adenoma
Causes of congenital hypothyroidism (Cretinism)
1. Maternal hypothyroidism 2. Thyroid agenesis 3. Thyroid dysgenesis (most common) 4. Iodine deficiency 5. Dyshormonogenetic goiter
Homer-Wrights rosettes
Neuroblastoma Medulloblastoma
Cholesterol in HYPERthyoroidism
HYPOcholesterolemia (increased LDL receptor expression)
Why is it important to have alpha-blockade before giving beta-blockers when treating pheochromocytoma?
Prevent a hypertensive crisis
Hyperthyroidism or hypothyroidism? Pretibial myxedema
Hyperthyroidism (Graves disease)
Histolog: Graves Disease
Tall, crowded follicular epithelial cells Scalloped colloid
Causes of nodular goiter
1. Toxic multi nodular goiter 2. Thyroid adenoma 3. Thyroid cancer 4. Thyroid cyst
Focal patches of hyper functioning follicular cells due to TSH receptor mutations (works independently of TSH): Graves Disease Toxic multi nodular Thyroid Storm
Toxic multinodular goiter Hot nodules are rarely malignant
True or false: Both hyperthyroidism and hypothyroidism present with proximal muscle weakness
True! But only hypothyroidism presents with increased CK.
Neuroblastoma vs. Wilms tumor
Neuroblastomas cross midline Wilms tumor: smooth and unilateral
Congenital hypothyroidism (Cretinism) 6 P's
1. Pot-bellied 2. Pale 3. Puffy face 4. Protruding umbilicus 5. Protuberant tongue 6. Poor brain development
Pathophysiology: Graves Disease
Thyroid-stimulating immunoglobulin (IgG) stimulates TSH receptors on thyroid and dermal fibroblasts.
What is the cause of death in thyroid storm?
Tachyarrhythmia
Other causes of hypothyroidism -- other than Hashimoto, congenital, de Quervain (subacute granulomatous), or Riedel thyroiditis.
1. Iodine deficiency 2. Goitrogens (Amiodarone, lithium) 3. Wolff-Chiakoff effect
Hypothyroidism following a flu-like illness (viral infection) Hashimoto thyroiditis Congenital hypothyroidism Graves Disease Riedel Thyroiditis Subacute granulomatous thyroiditis (de Quervain)
Subacute granulomatous thyroiditis (de Quervain) Self-limiting disease
Antithyroglobulin antibodies
Hashimoto thyroiditis
Over expression of N-myc oncogene Bombesin and NSE positive
Neuroblastoma
Symptoms of pheochromocytoma
5 P's: Pressure (increased BP) Pain (headache) Perspiration Palpitation (Tachycardia) Pallor
Antithyroid peroxidase (antimicrosomial) antibodies
Hashimoto thyroiditis
Treatment of pheochromocytoma
Phenoxybenzamine (irreversible alpha-antagonist) then beta-blockers BEFORE tumor resection.
Treatment of thyroid storm
4 P's: Propranolol (beta-blockers) Propylthiouracil Prednisolone (corticosteroids) Potassium iodide (Lugol iodine)
Type of hypothyroidism: 1. Increased ESR 2. Jaw pain 3. Very TENDER thyroid
Subacute granulomatous thyroiditis (de Quervain) de Quervain is associated with pain
HLA-DR5
Hashimoto thyroiditis
Hurthle cells (Lymphoid aggregates with germinal centers)
Hashimoto thyroiditis
Hypothyroidism or hyperthyroidism? Proximal muscle weakness Increased creatine kinase Myxedema (Facial/Periorbital) Dry, cool skin Coarse, brittle hair Dyspnea on exertion
Hypothyroidism
Incomplete treatment or untreated hyperthyroidism that worsens in the setting of acute stress (infection, trauma, surgery): Graves Disease Toxic multi nodular goiter Thyroid Storm
Thyroid storm
Cholesterol in hypothyroidism
HYPERcholesterolemia (Decreased LDL receptor expression)
Hashimoto thyroiditis
Antibodies: Antithyroid peroxidase (antimicrosomial) + antithyroglobulin HLA-DR5 Increased risk of non-Hodgkin lymphoma Enlarged, contender thyroid Hurthle cells
Section 3
(50 cards)
Undifferentiated/anaplastic carcinoma
Older patients Invades local structures. Poor prognosis p53 inactivation mutation
Which is the Gs alpha-subunit defect inherited by mother: Pseudohpyoparathyroidism type 1A Pseudopseudohypoparathyroidism
Pseudohypoparathyroidism type 1A
Treatment of thyroid cancer
Thyroidectomy
Secondary hyperparathyroidism pathophysiology
Chronic renal disease causing decreased vitamin D activation, leading to decreased calcium absorption and/or increased serum phosphate. Leads to hyperplasia of the parathyroid gland
Thyroid cancer from parafollicular C cells Produces calcitonin Sheets of cells in amyloid storm (stains with Congo red) MEN2A and 2B (RET mutations)
Medullary carcinoma
Ligation of superior laryngeal artery
Superior laryngeal nerves
Thyroid cancer with good prognosis. Invasion of thyroid capsule + vasculature Uniform follicles hematogenous spread common RAS mutation
Follicular carcinoma
Which Gs alpha-subunit defect is inherited by father: Pseudohypoparathyroidism type 1A Pseudopseudohypoparathyroidism
Pseudopseudohypoparathyroidism
Nelson Syndrome
Enlargement of ACTH-secreting pituitary adenoma (Cushing disease) after removing adrenals bilaterally to remove the increased cortisol response.)
Thyroid lymphoma is associated with what type of hypothyroid disease?
Hashimoto thyroidits
Osteitis fibrosa cystica
Cystic bone spaces filled with brown fibrous tissue Brown tumor consisting of osteoclasts and deposited hemosiderin from hemorrhages --> BONE PAIN
Refractory (autonomous) hyperparathyroidism resulting from chronic renal disease Increased PTH and calcium
Tertiary hyperparathyroidism
Osteitis fibrosa cystica is associated with: Primary hyperparathyroidism Secondary " Tertiary "
Primary hyperparathyroidism
MEN2A and MEN2B Papillary carcinoma Follicular carcinoma Medullary carcinoma
Medullary carcinoma
Trousseau sign
Occlusion of brachial artery with bP cuff (cuff the Triceps) --> carpal spasm
Findings in hypoparathyroidism
1. Tetany 2. Hypocalcemia 3. Hyperphosphatemia
Hot/toxic thyroid adenoma
Autonomous thyroid hormone production
Weakness Constipation (groans) Abdominal/flank pain (kidney stones, acute pancreatitis) Depression
Primary hyperparathyroidism Stones Bones Groans Psychiatric overtones
Cystic bone spaces filled with brown fibrous tissue Brown tumor consisting of osteoclasts and deposited hemosiderin from hemorrhages --> *BONE PAIN
Osteitis fibrosa cystica
Ligation of inferior thyroid artery
Recurrent laryngeal nerves
Orphan annie eyes
Empty-appearing nuclei with central clearing
Most common thyroid cancer . Excellent prognosis. Orphan Annie eyes. Psammoma bodies, nuclear grooves. RET + BRAF mutations. Child Irradiation
Papillary carcinoma
Presentation of Nelson syndrome
Hyper pigmentation Headaches Bitemporal hemianopia
Defective calcium-sensing receptor in multiple tissues -- requires higher than normal calcium levels required to suppress PTH Pseudohypoparathyroidims type 1A Pseudopseudohypoparathyroidism Familial hypocalciuric hypercalcemia
Familial hypocalciuric hypercalcemia Excessive renal calcium reuptake --> mild hypercalcemia + hypocalciuria Normal to increased PTH levels.
Nonfunctional pituitary adenoma
Silent Mass effect: - Bitemporal hmianopia - Hypopituitarism - Headache
Causes of primary hypoparathyroidism
Surgical resection Autoimmune DiGeorge Syndrome
Associated with RET and BRAF mutations: Papillary carcinoma Follicular carcinoma Medullary carcinoma
Papillary carcinoma
Causes of primary hyperparathyroidism
Hyperplasia Adenoma Carcinoma
Treatment for prolactinoma
Dopamin agonists (bromocriptine, cabergoline) Transsphenoidal resection
Functional pituitary adenoma
Based on hormone produced
Causes of PTH-independent hypercalcemia
Excess calcium intake Cancer
Benign solitary growth of thyroid
Thyroid adenoma
Inheritance: Pseudohypoparathyroidism type 1A (Albright hereditary osteodystrophy)
Autosomal dominant (Defect must be inherited from mother due to imprinting)
Difference between follicular carcinoma and follicular adenoma
Follicular carcinoma invades thyroid capsule and vascaulature
Renal osteodystrophy
Renal disease, leading to Secondary and tertiary hyperparathyroidism --> BONE LESIONS
Histology of thyroid adenoma
Follicular with absence of capsular/vascular invasion (unlike follicular carcinoma)
Causes of secondary hyperparathyroidism
Vitamin D deficiency Chronic renal failure
Complications of thyroidectomy
Hoarseness Hypocalcemia Transection of recurrent laryngeal + superior laryngeal nerve
Chvostek sign
tapping of facial nerve leads to contraction of facial muscles
Pathophysiology of pseudohypoparathyroidism type 1A (Albright hereditary osteodystrophy)
Defective Gs protein alpha-subunit causing end-organ resistance to PTH
Labs in hyperparathyroidism
Hypercalcemia, hypercalciuria (renal stones) Hypophosphatemia Increased PTH Increased ALP Increased cAMP in urine
Pseudopseudohypoparathyroidism
Shortened 4th/5th digits WITHOUT end-organ PTH resistance. Occurs when defective Gs protein alpha-subunit is inherited from father
Signs associated with hypoparathyroidism
Chvostek sign Trousseau sign
Cold thyroid adenoma
Nonfunctional
Thyrotoxicosis if patient with iodine deficiency and partially autonomous thyroid tissue is made iodine replete Opposite of Wolff-Chiakoff effect
Jod-Basedow Phenomenon
Pituitary adenoma
Benign tumor Most common: prolactinoma (from lactotrophs)
Hoarseness after thyroidectomy
Damage to recurrent laryngeal nerve
Pseudohypoparathyroidism type 1A (Albright hereditary osteodystrophy)
Kidneys unresponsive to PTH --> hypocalcemia despite increased PTH levels. Shortened 4th/5th digits Short stature Autosomal dominant
Hypocalcemia after thyroidectomy
Parathyroid gland
Associated with RAS mutation Papillary carcinoma Follicular carcinoma Medullary carcinoma
Follicular carcinoma
Section 4
(50 cards)
Causes of hypopituitarism
1. Non-secreting pituitary adenoma, craniopharyngioma 2. Sheehan Syndrome 3. Empty Sella Syndrome 4. Pituitary apoplexy 5. Brain injury 6. Radiation
Excess growth hormone in adults
Acromegaly
Treatment of acromegaly
Pituitary adenoma resection
Treatment of Nelson Syndrome
Pituitary irradiation Surgical resection
ADH antagonist
Demeclocycline
Diabetes: Fasting plasma glucose cutoff
> 126 MG/Dl Fasting > 8 hours
What medication can cause SIADH
Cyclophosphamide
Osmotic damage in diabetes mellitus is due to what?
Sorbitol accumulation in organs with aldose reductase - Decreased/absent sorbitol dehydrogenase Leads to: neuropathy, cataracts
Nephropathy in diabetes mellitus
Nodular glomerulosclerosis (Kimmelstiel-Wilson nodule): Progressive proteinuria (microalbuminuria)
Water deprivation test: Nephrogenic diabetes insipidus
Minimal change in urine osmolality, even after ADH analog administration
Complications of diabetes arise from what changes in the small and large vessels?
Non enzymatic glycation
Causes of nephrogenic diabetes insipidus
1. Hereditary (ADH receptor mutation) 2. Hypercalcemia 3. Hypokalemia 4. Lithium 5. ADH antagonist: demeclocycline
Water deprivation test: Central diabetes insipidus
Increased urine osmolality ONLY after administration of ADH analog
What is the most common cause of death in diabetes mellitus
Myocardial Infarction
Polydipsia Polyuria Polyphagia Weight loss DKA
Type 1 diabetes mellitus
Diagnosis for acromegaly
Increased IGF-1 Failure to suppress serum GH after oral glucose tolerance test Pituitary mass on brain MRI
Diabetes insipidus finding
Urine specific gravity <1.006 Serum osmolality >290 mOsm/kg Hyper osmotic volume contraction
Ischemic infarct of pituitary after postpartum bleeding Sheehan Syndrome Empty Sella Syndrome Pituitary Apoplexy
Sheehan Syndrome
Very low sodium levels in SIADH can lead to what?
1. Cerebral edema 2. Seizures
In SIADH, which is greater: Urine osmolality Serum osmolality
Urine osmolality
Type of hyponatremia in SIADH
Euvolemic hyponatremia
Diabetes: HbA1c diagnostic cutoff
> 6.5%
Treatment of central diabetes insipidus
ADH analog (desmopressin) Hydration
A somatostatin analog for treating acromegaly?
Octreotide
A growth hormone antagonist for treating acromegaly
Pegvisomant
Laron Syndrome pathophysiology
Defective growth hormone receptors, decreasing LINEAR growth - Increased GH - Decreased IGF-1
Treatment of nephrogenic DI
HCTZ Indomethacin Amiloride Hydration
Other causes of diabetes mellitus
GH Epinephrine Glucocorticoids
Atrophy or compression of pituitary. Common in obese women Sheehan Syndrome Empty Sella Syndrome Pituitary Apoplexy
Empty Sella Syndrome
Sudden severe headache, biteomporal hemianopia or diplopia due to CN III palsy. Features of hypopituitarism
Pituitary Apoplexy
Treatment of SIADH
1. Fluid restriction 2. Salt tablets 3. IV hypertonic saline 4. Diuretics 5. Conivaptan 6. Tolvaptan 7. Demeclocylcine
Large vessel non enzymatic glycation in diabetes mellitus
Atherosclerosis CAD Peripheral vascular occlusive disease Gangrene (limb loss) Cebreovascular disease MI
Intense thirst Polyuria Inability to concentrate urine
Diabetes insipidus
Failure to lactate. No menstruation. Cold intolerance Sheehan Syndrome Empty Sella Syndrome Pituitary Apoplexy
Sheehan Syndrome
Water deprivation test
No water intake for 2-3 hours. Measurements of urine volume + osmolarity + sodium concentration + osmolarity. ADH analog (desmopressin) administered if: -Serum osmolality > 295-300 mOsm/kg - Plasma Na+ >145 - Urine osmolality doesn't rise despite a rising plasma osmolality
Small vessel non enzymatic glycation in diabetes mellitus
Diffuse thickening of basement membrane, causing: 1. Retinopathy (hemorrhage, exudates, micro aneurysms, vessel proliferation) 2. Glaucoma 3. Neuropathy 4. Nephropathy 5. Arteriosclerosis
Response to SAIDH
Water retention leads to; 1. Decreased aldosterone 2. Increased ANP and BNP 3. Urinary Na+ secretion = normalization of extracellular fluid volume --> euvolemic nyonatremia.
If pituitary adenoma resection doesn't work for treating acromegaly, what can you use?
Octreotide (somatostatin analog) Pegvisomant (growth hormone receptor antagonist)
Characteristics of SIADH
1. Excessive free water retention 2. Euvolemic hyponatremia with urinary Na+ excretion 3. Urine osmolality > serum osmolality
Sudden hemorrhage of pituitary gland. Usually with existing pituitary adenoma. Sudden headache, visual impairment, features of hypopituitarism Sheehan Syndrome Empty Sella Syndrome Pituitary Apoplexy
Pituitary Apoplexy
Short height Small head circumference Saddle nose with prominent forehead Delayed skeletal maturation Small genitalia
Laron Syndrome (Dwarfism)
Large tongue with deep furrows Deep voice Large hands and feet Coarsening of facial features with aging Frontal bossing Diaphoresis Impaired glucose tolerance (insulin resistance) Increased risk of colorectal polyps and cancer
Acromegaly
Craniopharyngioma can cause what?
Hypopituitarism
Acromegaly is typical caused by what?
Pituitary adenoma
Acromegaly results in an increased risk for what?
Colorectal polyps Cancer
Why is it important to correct sodium levels slowly in SIADH?
Prevent osmotic demyelination syndrome (central pontine myelinolysis)
Syndrome of inappropriate ADH section (SIADH) causes
1. Ectopic ADH 2. CNS disorder/head trauma 3. Pulmonary disease 4. Drugs (cyclophosphamide)
Treatment of hypopituitarism
Hormone replacement therapy: - corticosteroids - thyroxine - sex steroids - human growth hormone
Causes of central diabetes insipidus
1. Pituitary tumor 2. Autoimmune 3. Trauma 4. Surgery 5. Ischemic encephalopathy 6. Idiopathic
Polydipsia Polyuria Polyphagia Weight loss Hyperosmolar coma
Diabetes mellitus type 2
Section 5
(50 cards)
Gastrin-secreting tumor (gastrinoma) of pancreas OR duodenum, leading *recurrent ulcers in duodenum + jejunum) due to acid hyper secretion Presents with abdominal pain and diarrhea (malabsorption)
Zollinger-Ellison syndrome
Labs in carcinoid syndrome
Urine: increased 5-HIAA (hydroxyindoleacetic acid) Decreased niacin
Pituitary tumors Pancreatic endocrine tumors Parathyroid adenomas Makes up: - MEN1 - MEN2A - MEN2B
MEN 1 3 P's
Diabetes Type 1 is associated with what HLA?
HLA-DR3 HLA-DR4
Zollinger-Ellison syndrome leads to ulcers found in what part of the small intestine?
Duodenum Jejunum
Decreased blood glucose Increased C-peptide Found in: Glucagonoma Insulinoma Somatostatinoma
Insulinoma
Complications of diabetic ketoacidosis
1. Mucormycosis (Rhizomes infection) 2. Cerbrela edema 3. Cardiac arrhythmias (hyperkalemia) 4. Heart failure
What is the most common malignancy in the small intestine?
Carcinoid syndrome
Presents with diabetes/glucose intolerance, steatorrhea, gallstones Glucagonoma Insulinoma Somatostatinoma
Somatostatinoma
Diabetic ketoacidosis: Metabolic acidosis Metabolic alkalosis
Metabolic acidosis
What is carcinoid syndrome caused by?
Carcinoid tumors from neuroendocrine cells. Especially metastatic small bowel tumors that secrete lots of serotonin.
Symptoms of hyperosmolar hyperglycemia nonketotic syndrome
This, polyuria, lethargy Focal neurological deficits (seizures) --> progress to coma and death if untreated
Treatment of hyperosmolar hyperglycemia nonketotic syndrome
IV fluids Insulin therapy
Labs: Diabetic ketoacidosis
Hyperglycemia Increased H+ Decreased HCO3- Increased blood ketone levels Leukocytosis Hyperkalemia
Pathophysiology: Hyperosmolar hyperglycemia nonketotic syndrome
Hyperglycemia --> excessive osmotic diuresis --> dehydration --> onset of hyperosmolar hyperglycemia nonketotic syndrome
Glucagonoma presentation
Tumor of pancreatic alpha cells Dermatitis (necrolytic migratory erythema) Diabetes DVT Declining weight gain Depression
treatment of glucagonoma
Octreotide Surgery
Associated with MEN 1 syndrome: Glucagonoma Insulinoma Somatostatinoma
Insulinoma
Signs/Symptoms in diabetic ketoacidosis: DKA is Deadly
Delirium/psychosis Kussmaul respirations (rapid/deep breathing) Abdominal pain/nausea/vomiting Dehydration Fruity breath odor (exhaled acetone)
Genetic predisposition is strong in: Diabetes type 1 Diabetes type 2
Diabetes type 2
Secretin stimulation test: Zollinger-Ellison syndrome
Positive -- administration of secretin maintains elevation of gastrin levels. (Secretin normally inhibits gastrin release)
Diabetic ketoacidosis is usually due to what?
1. Increased insulin requirements due to stress 2. Noncompliance
Is acidosis found in hyperosmolar hyperglycemia nonketotic syndrome?
No! No ketones are produced...inhibited by presence of insulin
Recurrent diarrhea Cutaneous flushing Asthmatic wheezing right-sided valvular heart disease Pellagra
Carcinoid syndrome
What right-sided valvular heart disease is found in carcinoid syndrome?
Tricuspid regurgitation Pulmonic stenosis
Treatment of diabetic ketoacidosis
1. IV fluids 2. IV insulin 3. K+ (restore intracellular stores) Glucose (if needed to prevent hypoglycemia)
Treatment of carcinoid syndrome
Surgical resection Somatostatin analog (ocreotide)
Necrolytic migratory erythema is found in: Glucagonoma Insulinoma Somatostatinoma
Glucagonoma
insulinoma
Tumor of pancreatic beta cells --> overproduction of insulin --> hypoglycemia
Hyperosmolar hyperglycemia nonketotic syndrome
State of profound hyperglycemia-induced dehydration Increased serum osmolarity
Pathophysiology of diabetic ketoacidosis
Excess fat breakdown Increased ketogenesis from free fatty acids --> ketone bodies
Hyperosmolar hyperglycemia nonketotic syndrome is commonly seen in what kind of patients?
Elderly type 2 diabetics with limited ability to drink
Symptoms of hypogylcemia
Lethargy Syncope Diplopia
Diabetes: 2-hour oral glucose intolerance test cutoff
> 200 mg/dL 2 hours after consumption of 75g of glucose in water
MEN 1 (menin) Tumor suppressor Oncogene
Tumor suppressor
Treatment of insulinoma
Surgical resection
Carcinoid syndrome: Rule of 1/3s
1/3 metastasize 1/3 present with 2nd malignancy 1/3 are multiple
MEN (multiple endocrine neoplasias) inheritance pattern
Autosomal dominant All MEN are dominant.
Increased resistance to insulin, progressive pancreatic beta-cell failure Diabetes Type 1 Diabetes Type 2
Diabetes type 2
Glutamic acid decarboxylase antibodies
Diabetes mellitus type 1
treatment of somatostatinoma
Surgical resection Somatostatin analog (ocretotide)
Autoimmune destruction of beta-islet cells Diabetes Type 1 Diabetes Type 2
Diabetes type 1
MEN 1 (menin) is found on what chromosome
Chromosome 11
Whipple triad
1. Low blood glucose 2. Symptoms of hypoglycemia (lethargy, syncope, diplopia) 3. Resolution of symptoms after normalization of glucose Seen in insulinoma
Histology: Islet leukocytic infiltrate Diabetes type 1 Diabetes type 2
Diabetes type 1
Histology: Islet amyloid polypeptide (IAPP) deposites
Diabetes type 2
Zollinger-Ellison syndrome is associated with MEN 1 MEN2A MEN2B
MEN 1
Sinatistatubina
Tumor of pancreatic delta cells --> overproduction of somatostatin --> Decreased: 1. Secretin 2. Cholecystokinin 3. Glucagon 4. Insulin 5. Gastrin
Ketone bodies in diabetic ketoacidosis
Beta-hydroxybutyrate > acetoacetate
Carcinoid syndrome is seen in: Metastatic bowel tumors Tumors confined in GI tract
Metastatic bowel tumors.
Section 6
(6 cards)