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93 Cards in this Set
- Front
- Back
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What is Cushing's Syndrome?
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=increased cortisol due to a variety of causes
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Etiologies of Cushing's Syndrome
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1) Cushing's Disease
=i.e. a pituitary adenoma =INCREASED ACTH 2) Primary adrenal hyperplasia/neoplasia =DECREASED ACTH 3) Ectopic ACTH production =i.e. small cell lung cancer =INCREASED ACTH 4) Iatrogenic =i.e. chronic steroids =DECREASED ACTH |
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Clinical Picture of Cushing's Syndrome
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-HTN
-truncal obesity -thin extremities -buffalo hump--osteoporosis -moon facies -purple striae -thinning skin -hyperglycemia (=insulin resistance) -amenorrhea -immune suppression COLOR IMAGE 70 |
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How do you test for Cushings?
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**Dexamethasone (=glucocorticoid analog)Suppression Test
=IF the person is healthy --> DECREASED cortisol after a low dose =IF the person has an ACTH-producing tumor --> INCREASED cortisol after a LOW dose and DECREASED cortisol after a HIGH dose =IF someone has a cortisone-producing tumor --> INCREASED cortisol after a LOW and HIGH dose |
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What is Primary Hyperaldosteronism?
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**Called Conn's Syndrome
=caused by an aldosterone-secreting tumor **Results in: -HTN -HypOkalemia -Metabolic alkalosis -LOW plasma renin |
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What is Secondary Hyperaldosteronism?
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**Can be due to:
=renal artery stenosis =chronic renal failure =CHF =cirrhosis =nephrotic syndrome **Kidney perception of LOW intravascular volume --> results in an OVERACTIVE renin-angiotensin system =i.e. is associated w/ HIGH plasma renin |
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Treatment of Hyperaldosteronism
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**Spironolactone
=K+sparing diuretic =works by acting as an aldosterone ANTAGONIST |
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What is Addison's Disease?
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=Primary deficiency of ALDOSTERONE and CORTISOL due to adrenal atrophy
**Characterized by ADRENAL ATROPHY and ABSENCE of HORMONE PRODUCTION =involves all 3 cortical divisions |
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Symptoms of Addison's Disease.
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1) Hypotension
=hyponatremic volume contraction 2) Skin hyperpigmentation =due to MSH --> a by-product of increased ACTH production from POMC (proopriomelanocortin) |
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How to distinguish PRIMARY from SECONDARY insufficiency.
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=secondary insufficiency has NO skin hyperpigmentation
(=DECREASED pituitary ACTH production) |
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What is a Pheochromocytoma?
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**The most common tumor of the adrenal medulla in adults
=derived from CHROMAFFIN CELLS (arise from neural crest) **Pheochromocytomas may be associated w/ neurofibromatosis and MEN types II and III COLOR IMAGE 69 |
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What do pheochromocytomas secrete?
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=epinephrine, NE, and dopamine
=urinary VMA levels + plasma catecholamines are ELEVATED |
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Symptoms:
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**Symptoms occur in spells--relapse and remit
=5 P's: Pressure = elevated BP Pain = headache Perspiration = tachycardia Palpitations Pallor |
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RULE OF 10's
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10% malignant
10% bilateral 10% extra-adrenal 10% calcify 10% kids 10% familial |
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Treatment of Pheochromocytoma
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=alpha antagonists ESP. phenoxybenzamine (a nonselective, IRREVERSIBLE alpha-blocker)
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Neuroblastoma
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=most common tumor of the adrenal medulla in children
**can occur anywhere along the sympathetic chain |
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Multiple Endocrine Neoplasias (MEN)
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Types:
=MEN I =MEN II =MEN III **ALL MEN syndromes have autosomal dominant inheritance. **MEN II and III are associated w/ the ret gene |
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MEN Type I
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=Wermer's Syndrome
**Involves the 3 "P" organs --> Pancreas, Pituitary, and Parathyroid 1) Pancreas =Zollinger-Ellison Syndrome =Insulinomas =VIPomas 2) Parathyroid tumors 3) Pituitary tumors |
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Common Presentation of MEN I
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=kidney stones + stomach ulcers
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MEN Type II
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=Sipple's Syndrome
-Medullary carcinoma of the thyroid -Pheochromocytoma -Parathyroid tumor |
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MEN Type III
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(=formerly MEN IIb)
-medullary carcinoma of the thyroid -pheochromocytoma -oral and intestinal ganlioneuromatosis (=mucosal neuromas) |
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Symptoms of Hypothyroidism
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1) Cold intolerance
2) Hypoactivity 3) Weight gain 4) Fatigue, lethargy, weakness 5) Decreased appetite 6) Constipation 7) Decreased reflexes 8) Myxedema (=facial/periorbital) 9) Dry, cool skin 10) Coarse, brittle hair |
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Symptoms of Hyperthyroidism
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1) Heat intolerance
2) Hyperactivity 3) Weight loss 4) Chest pain/palpitations 5) Arrhythmias 6) Diarrhea 7) Increased reflexes 8) Warm, moist skin 9) Fine hair |
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How do you diagnose primary hypothyroidism?
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=INCREASED TSH --> a sensitive test for primary hypothyroidism only
=DECREASED total T4 =DECREASED free T4 =DECREASED T3 uptake |
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How do you diagnose primary hyperthyroidism?
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=DECREASED TSH
=INCREASED total T4 =INCREASED free T4 =INCREASED T3 uptake |
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What is Grave's Disease?
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=Autoimmune HYPERthyroidism w/ thyroid-stimulating/TSH receptor antibodies
**Type II HYPERSENSITIVITY |
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Symptoms of Grave's Disease.
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=PROPTOSIS
=EOM swelling =Pretibial myxedema =DIFFUSE GOITER **Often presents during stress--i.e. childbirth COLOR PLATE 71 |
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Riedel's Thyroiditis
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=thyroid replaced by fibrous tissue
**HYPOTHYROID** |
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Hashimoto's Thyroiditis
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=Autoimmune disorder resulting in HYPOTHYROIDISM
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What are the symptoms of Hashimoto's Thyroiditis?
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**Slow course.
=moderately enlarged, nontender thyroid =LYMPHOCYTIC infiltrate w/ germinal centers =Antimicrosomal and antithyroglobulin antibodies |
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What is Subacute Thyroiditis?
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=called "de Quervain's"
**Self-limited HYPOTHYROIDISM often following a flu-like illness =Elevated ESR =Early inflammation =Jaw pain =VERY tender thyroid gland **note: may actually be HYPERthyroid early in the course |
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Thyroid Cancer
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1) Papillary Carcinoma
2) Follicular Carcinoma 3) Medullary Carcinoma 4) Undifferentiated/ anaplastic |
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Papillary Carcinoma
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=Most common --> EXCELLENT prognosis
**"ground glass" nuclei **psammoma bodies |
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What is a psammoma body?
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=round collection of calcium
**Seen in 3 Main Places: =Papillary thyroid cancecr =Serous cystadenocarcinoma--most common type of ovarian cancer =Meningiomas |
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Follicular Carcinoma
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=good prognosis
**Uniform follicles |
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Medullary carcinoma
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**from parafollicular "C" cells
=produces CALCITONIN =sheets of cells in amyloid stroma **Associated w/ MEN types II and III |
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Undifferentiated/Anaplastic
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=Older patients
**VERY poor prognosis |
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Cretinism
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**Can be:
1) Endemic 2) Sporadic =Cretin means "Christlike" --> those affected were considered SO mentally retarded as to be incapable of sinning. **Still common in CHINA |
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Endemic Cretinism
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**Occurs wherever endemic goiter is prevalent
=lack of dietary iodine --> most common cause of goiter |
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Sporadic Cretinism
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**Caused by a defect in T4 formation OR developmental failure in thyroid formation
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Findings in Cretinism:
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=pot-bellied, pale, puffy-faced child w/ a protruding umbilicus AND protuberant tongue
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Cause of Acromegaly
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**Excess GH in adults.
Recall: =increased GH is normal in stress, exercise, and hypoglycemia |
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Findings in Acromegaly
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1) Large tongue w/ deep furrows
2) Deep voice 3) Large hands and feet 4) Course facial features 5) Impaired glucose tolerance (=insulin resistance) |
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Increased GH in children =
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Gigantism
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Treatment of Acromegaly
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=Octreotide
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Hyperparathyroidism
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**Can be primary OR secondary
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What are the cause and lab findings in Primary Hyerparathyroidism?
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**Usually an ADENOMA
=HYPERcalcemia =HYPERcalciuria (can lead to renal stones) =HYPOphosphatemia =INCREASED PTH =INCREASED cAMP in urine |
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How do people w/ primary hyperparathyroidism present?
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**Often asymptomatic OR may present w/ WEAKNESS + CONSTIPATION (="groans")
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What are the cause and lab findings in Secondary Hyperparathyroidism?
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=Secondary hyperplasia due to decreased serum Ca+ --> usually in chronic renal disease
Findings: =HYPOcalcemia =HYPERphosphatemia =INCREASED PTH **recall: the KIDNEY is the primary means of excreting phosphate |
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What is Osteitis Fibrosa Cystica?
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=Von Recklinhausen's Syndrome
**Caused by hyperparathyroidism --> due to the rapid mobilization of calcium =cystic bone spaces (=increased bone reabsorption) filled w/ brown fibrous tissue =can cause BONE PAIN, pathologic fractures, + bowing of the bones |
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What is Renal Osteodystrophy?
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=Bone lesions secondary to hyperparathyroidism due to RENAL DISEASE
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What are the symptoms of Hypoparathyroidism?
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=Hypocalcemia + tetany (=due to hypocalcemia)
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Causes of Hypoparathyroidism.
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1) Accidental surgical excision--i.e. in thyroid surgery
2) DiGeorge Syndrome |
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Signs of Tetany.
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1) Chvostek's Sign
=Tap facial nerve --> contraction of facial muscles 2) Trousseau's Sign =Occlusion of brachial artery w/ BP cuff --> carpal spasm |
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Wait...DiGeorge Syndrome? I thought that was a disease characterized by an absent thymus...
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IT IS!
But, the thymus, parathyroid glands, AND heart all derive from the same embroyonic structure. |
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What are the causes of Hypercalcemia?
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CHIMPANZEES
=Calcium ingestion (=milk-alkali syndrome) =Hyperparathyroid =Hyperthyroid =Iatrogenic (=thiazides) =Multiple myeloma =Paget's disease =Addison's disease =Neoplasms =Zollinger-Ellison Syndrome =Excess vitamin D =Excess vitamin A =Sarcoidosis |
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ACUTE Manifestations
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-Polydipsia
-Polyuria -Polyphagia (=excessive eating) -Weight loss -Diabetic ketoacidosis--DKA (=type I) -Hyperosmolar coma (=type II) -Unopposed secretion of GH and Epi --> EXACERBATES hyperglycemia |
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CHRONIC Manifestations
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1) Nonenzymatic Glycosylation
2) Osmotic Damage |
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What are the manifestations of nonenzymatic glycosylation?
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1) Small Vessel Disease --> diffuse thickening of the basement membrane that can lead to:
=Retinopathy (i.e. hemorrhage, exudates, microaneurysms, vessel proliferation) =Glaucoma =Nephropathy (i.e. nodular sclerosis, progressive proteinuria, chronic renal failure) =Arteriosclerosis leading to HTN 2) Large Vessel Atherosclerosis =CAD =Peripheral vascular occlusive disease + gangrene =Cerebrovascular disease |
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What are the effects of Osmotic Damage?
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1) Neuropathy
=motor, sensory, and autonomic degeneration 2) Cataracts =sorbitol accumulation |
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Tests for DM
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=Fasting serum glucose
=Glucose tolerance test =HbA1c --> measures LONG-TERM diabetic control |
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Type I vs. Type II Diabetes Mellitus
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Type I = JUVENILE ONSET (IDDM)
Type II = ADULT ONSET (NIDDM) |
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Primary Defect:
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I = Viral or immune destruction of B-cells (COLOR IMAGE 67)
II = Increased RESISTANCE to insulin |
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Insulin necessary in treatment?
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I = ALWAYS
II = Sometimes |
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Age
=exceptions commonly occur! |
I = <30 y.o.
II = >40 y.o. |
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Associated w/ Obesity?
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I = NO
II = YES |
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Genetic Predisposition?
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I = Weak, polygenic
II = Strong, polygenic |
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Association w/ HLA System?
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I = Yes --> HLA-DR3 and 4
II = NO |
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Glucose intolerance?
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I = SEVERE
II = Mild to moderate |
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Ketoacidosis?
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I = Common
II = Rare |
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What is ketoacidosis?
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**Despite possibly HIGH levels of circulating glucose, the liver will act as though the body is STARVING itself IF insulin levels are low/absent
=SO, in starvation situations, the liver produces KETONE BODIES for fuel --> IF large quantities of ketone bodies are produced = ketosis =positive charge of the ketone bodies causes DECREASED (acidic) blood pH =EXTREME excess of ketones --> KETOACIDOSIS |
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B-cell numbers in the islets?
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I = DECREASED
II = Variable |
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Serum insulin level?
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I = DECREASED
II = Variable |
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Classic symptoms of polyuria, polydipsia, thirst, and weight loss?
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I = Common
II = Sometimes |
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SO, again, what is DTA?
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**One of the most impt. complications of type I diabetes
=USUALLY due to an INCREASE in insulin requirements from an INCREASE in stress (i.e. infection) =Excess FAT BREAKDOWN + increased ketogenesis from the INCREASE in free FATTY acids --> made into KETONE BODIES |
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Signs/Symptoms of DTA:
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1) Kussmaul respirations
=rapid/deep breathing 2) Hyperthermia 3) N/V and abdominal pain 4) Psychosis/dementia 5) Dehydration 6) FRUITY BREATH ODOR = due to exhaled acetone |
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Labs of someone w/ DTA:
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=HYPERglycemia
=INCREASED H+ and DECREASED HCO3- --> METABOLIC ACIDOSIS =INCREASED ketone blood levels =Leukocytosis =HYPERkalemia but depleted intracellular K+ |
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Complications:
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=life-threatening mucormycosis
=Rhizopus infection =cerebral edema =cardiac arrhythmias =heart failure |
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Treatment:
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-Fluids
= lower osmolarity of blood -Insulin =forces glucose and K into cells -Potassium **Glucose if necessary to prevent HYPOglycemia |
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What is Diabetes Insipidus?
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**Excretion of large amounts of DILUTE urine
=characterized by intensive thirst + polyuria TOGETHER w/ an inability to concentrate urine due to: 1) A LACK of ADH --> CENTRAL DI =pituitary tumor =trauma or surgery =histiocytosis X 2) Lack of renal RESPONSE to ADH --> NEPHROGENIC DI =Heriditary OR =Secondary to hypercalcemia, lithium, OR demeclocycline |
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Diagnosis:
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**Water deprivation test
=urine osmolality DOES NOT increase! |
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Findings:
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**Urine specific gravity < 1.006
=basically, urine specific gravity is measuring the [] of solutes in the urine **Serum osmolality > 290 mOsm/L |
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Treatment:
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1) Adequate fluid intake.
2) For CENTRAL DI: =Intranasal desmopression (=ADH analog) 3) For NEPHROGENIC DI: =Hydrochlorothiazide =Indomethacin =Amiloride |
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What is SIADH?
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**Syndrome of inappropriate ADH secretion:
1) Excessive water retention 2) Hyponatremia 3) Urine osmolarity > serum osmolarity |
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Causes of SIADH:
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1) Ectopic ADH
= small cell lung cancer 2) CNS Disorders/head trauma 3) Pulmonary disease 4) Drugs =ex. cyclophasphamide |
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Where is ADH made?
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**Made in the hypothalamus --> released into the posterior pituitary
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Complications:
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**Very low serum sodium levels can lead to SEIZURES
=correct slowly |
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Treatment:
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**Treat w/ demeclocycline OR H20 restriction
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What is carcinoid syndrome?
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=rare syndrome caused by CARCINOID tumors (=derived from neuroendocrine cells in the GI tract --> carcinoid tumors can occur anywhere along the GI tract
=SYMPTOMS of carcinoid tumors result from metastatic small bowel tumors which secrete HIGH LEVELS of SEROTONIN (5-HT) **NOW...you will NOT see carcinoid syndrome symptoms if the tumor is LIMITED to the GI tract =5-HT undergoes first-pass metabolism in the liver =it is not until the tumor has metastasized to the liver **MOST COMMON TUMOR OF THE APPENDIX! |
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Symptoms of Carcinoid Syndrome
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1) Recurrent diarrhea
2) Cutaneous flushing =does NOT result from the secretion of serotonin BUT from the secretion of kallikrein --> catalyzes conversion of kininogen to BRADYKININ = potent VASODILATOR 3) Asthmatic wheezing 4) Right-sided valvular disease **You will see increased 5-HIAA (=main metabolite of serotonin) in the urine |
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Rule of 1/3's:
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1/3 metastasize
1/3 present w/ 2nd malignancy 1/3 multiple |
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Treatment:
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Octreotide
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Zollinger-Ellison Syndrome
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=Gastrin-secreting tumor of the pancreas OR duodenum
=Causes recurrent ulcers **May be associated w/ MEN Type I |
