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93 Cards in this Set

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What is Cushing's Syndrome?
=increased cortisol due to a variety of causes
Etiologies of Cushing's Syndrome
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
Clinical Picture of Cushing's Syndrome
-HTN
-truncal obesity
-thin extremities
-buffalo hump--osteoporosis
-moon facies
-purple striae
-thinning skin
-hyperglycemia (=insulin resistance)
-amenorrhea
-immune suppression

COLOR IMAGE 70
How do you test for Cushings?
**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
What is Primary Hyperaldosteronism?
**Called Conn's Syndrome

=caused by an aldosterone-secreting tumor

**Results in:
-HTN
-HypOkalemia
-Metabolic alkalosis
-LOW plasma renin
What is Secondary Hyperaldosteronism?
**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
Treatment of Hyperaldosteronism
**Spironolactone
=K+sparing diuretic
=works by acting as an aldosterone ANTAGONIST
What is Addison's Disease?
=Primary deficiency of ALDOSTERONE and CORTISOL due to adrenal atrophy

**Characterized by ADRENAL ATROPHY and ABSENCE of HORMONE PRODUCTION
=involves all 3 cortical divisions
Symptoms of Addison's Disease.
1) Hypotension
=hyponatremic volume contraction

2) Skin hyperpigmentation
=due to MSH --> a by-product of increased ACTH production from POMC (proopriomelanocortin)
How to distinguish PRIMARY from SECONDARY insufficiency.
=secondary insufficiency has NO skin hyperpigmentation

(=DECREASED pituitary ACTH production)
What is a Pheochromocytoma?
**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
What do pheochromocytomas secrete?
=epinephrine, NE, and dopamine

=urinary VMA levels + plasma catecholamines are ELEVATED
Symptoms:
**Symptoms occur in spells--relapse and remit

=5 P's:

Pressure = elevated BP
Pain = headache
Perspiration = tachycardia
Palpitations
Pallor
RULE OF 10's
10% malignant
10% bilateral
10% extra-adrenal
10% calcify
10% kids
10% familial
Treatment of Pheochromocytoma
=alpha antagonists ESP. phenoxybenzamine (a nonselective, IRREVERSIBLE alpha-blocker)
Neuroblastoma
=most common tumor of the adrenal medulla in children

**can occur anywhere along the sympathetic chain
Multiple Endocrine Neoplasias (MEN)
Types:
=MEN I
=MEN II
=MEN III

**ALL MEN syndromes have autosomal dominant inheritance.

**MEN II and III are associated w/ the ret gene
MEN Type I
=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
Common Presentation of MEN I
=kidney stones + stomach ulcers
MEN Type II
=Sipple's Syndrome

-Medullary carcinoma of the thyroid
-Pheochromocytoma
-Parathyroid tumor
MEN Type III
(=formerly MEN IIb)

-medullary carcinoma of the thyroid
-pheochromocytoma
-oral and intestinal ganlioneuromatosis (=mucosal neuromas)
Symptoms of Hypothyroidism
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
Symptoms of Hyperthyroidism
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
How do you diagnose primary hypothyroidism?
=INCREASED TSH --> a sensitive test for primary hypothyroidism only

=DECREASED total T4
=DECREASED free T4
=DECREASED T3 uptake
How do you diagnose primary hyperthyroidism?
=DECREASED TSH

=INCREASED total T4
=INCREASED free T4
=INCREASED T3 uptake
What is Grave's Disease?
=Autoimmune HYPERthyroidism w/ thyroid-stimulating/TSH receptor antibodies

**Type II HYPERSENSITIVITY
Symptoms of Grave's Disease.
=PROPTOSIS
=EOM swelling
=Pretibial myxedema
=DIFFUSE GOITER

**Often presents during stress--i.e. childbirth

COLOR PLATE 71
Riedel's Thyroiditis
=thyroid replaced by fibrous tissue

**HYPOTHYROID**
Hashimoto's Thyroiditis
=Autoimmune disorder resulting in HYPOTHYROIDISM
What are the symptoms of Hashimoto's Thyroiditis?
**Slow course.

=moderately enlarged, nontender thyroid
=LYMPHOCYTIC infiltrate w/ germinal centers
=Antimicrosomal and antithyroglobulin antibodies
What is Subacute Thyroiditis?
=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
Thyroid Cancer
1) Papillary Carcinoma
2) Follicular Carcinoma
3) Medullary Carcinoma
4) Undifferentiated/ anaplastic
Papillary Carcinoma
=Most common --> EXCELLENT prognosis

**"ground glass" nuclei
**psammoma bodies
What is a psammoma body?
=round collection of calcium

**Seen in 3 Main Places:
=Papillary thyroid cancecr
=Serous cystadenocarcinoma--most common type of ovarian cancer
=Meningiomas
Follicular Carcinoma
=good prognosis

**Uniform follicles
Medullary carcinoma
**from parafollicular "C" cells
=produces CALCITONIN
=sheets of cells in amyloid stroma

**Associated w/ MEN types II and III
Undifferentiated/Anaplastic
=Older patients

**VERY poor prognosis
Cretinism
**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
Endemic Cretinism
**Occurs wherever endemic goiter is prevalent
=lack of dietary iodine --> most common cause of goiter
Sporadic Cretinism
**Caused by a defect in T4 formation OR developmental failure in thyroid formation
Findings in Cretinism:
=pot-bellied, pale, puffy-faced child w/ a protruding umbilicus AND protuberant tongue
Cause of Acromegaly
**Excess GH in adults.

Recall:
=increased GH is normal in stress, exercise, and hypoglycemia
Findings in Acromegaly
1) Large tongue w/ deep furrows
2) Deep voice
3) Large hands and feet
4) Course facial features
5) Impaired glucose tolerance (=insulin resistance)
Increased GH in children =
Gigantism
Treatment of Acromegaly
=Octreotide
Hyperparathyroidism
**Can be primary OR secondary
What are the cause and lab findings in Primary Hyerparathyroidism?
**Usually an ADENOMA

=HYPERcalcemia
=HYPERcalciuria (can lead to renal stones)
=HYPOphosphatemia
=INCREASED PTH
=INCREASED cAMP in urine
How do people w/ primary hyperparathyroidism present?
**Often asymptomatic OR may present w/ WEAKNESS + CONSTIPATION (="groans")
What are the cause and lab findings in Secondary Hyperparathyroidism?
=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
What is Osteitis Fibrosa Cystica?
=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
What is Renal Osteodystrophy?
=Bone lesions secondary to hyperparathyroidism due to RENAL DISEASE
What are the symptoms of Hypoparathyroidism?
=Hypocalcemia + tetany (=due to hypocalcemia)
Causes of Hypoparathyroidism.
1) Accidental surgical excision--i.e. in thyroid surgery

2) DiGeorge Syndrome
Signs of Tetany.
1) Chvostek's Sign
=Tap facial nerve --> contraction of facial muscles

2) Trousseau's Sign
=Occlusion of brachial artery w/ BP cuff --> carpal spasm
Wait...DiGeorge Syndrome? I thought that was a disease characterized by an absent thymus...
IT IS!

But, the thymus, parathyroid glands, AND heart all derive from the same embroyonic structure.
What are the causes of Hypercalcemia?
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
ACUTE Manifestations
-Polydipsia
-Polyuria
-Polyphagia (=excessive eating)
-Weight loss
-Diabetic ketoacidosis--DKA (=type I)
-Hyperosmolar coma (=type II)
-Unopposed secretion of GH and Epi --> EXACERBATES hyperglycemia
CHRONIC Manifestations
1) Nonenzymatic Glycosylation

2) Osmotic Damage
What are the manifestations of nonenzymatic glycosylation?
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
What are the effects of Osmotic Damage?
1) Neuropathy
=motor, sensory, and autonomic degeneration

2) Cataracts
=sorbitol accumulation
Tests for DM
=Fasting serum glucose
=Glucose tolerance test
=HbA1c --> measures LONG-TERM diabetic control
Type I vs. Type II Diabetes Mellitus
Type I = JUVENILE ONSET (IDDM)

Type II = ADULT ONSET (NIDDM)
Primary Defect:
I = Viral or immune destruction of B-cells (COLOR IMAGE 67)

II = Increased RESISTANCE to insulin
Insulin necessary in treatment?
I = ALWAYS

II = Sometimes
Age
=exceptions commonly occur!
I = <30 y.o.

II = >40 y.o.
Associated w/ Obesity?
I = NO

II = YES
Genetic Predisposition?
I = Weak, polygenic

II = Strong, polygenic
Association w/ HLA System?
I = Yes --> HLA-DR3 and 4

II = NO
Glucose intolerance?
I = SEVERE

II = Mild to moderate
Ketoacidosis?
I = Common

II = Rare
What is ketoacidosis?
**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
B-cell numbers in the islets?
I = DECREASED

II = Variable
Serum insulin level?
I = DECREASED

II = Variable
Classic symptoms of polyuria, polydipsia, thirst, and weight loss?
I = Common

II = Sometimes
SO, again, what is DTA?
**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
Signs/Symptoms of DTA:
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
Labs of someone w/ DTA:
=HYPERglycemia

=INCREASED H+ and DECREASED HCO3- --> METABOLIC ACIDOSIS

=INCREASED ketone blood levels

=Leukocytosis

=HYPERkalemia but depleted intracellular K+
Complications:
=life-threatening mucormycosis
=Rhizopus infection
=cerebral edema
=cardiac arrhythmias
=heart failure
Treatment:
-Fluids
= lower osmolarity of blood

-Insulin
=forces glucose and K into cells

-Potassium

**Glucose if necessary to prevent HYPOglycemia
What is Diabetes Insipidus?
**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
Diagnosis:
**Water deprivation test
=urine osmolality DOES NOT increase!
Findings:
**Urine specific gravity < 1.006

=basically, urine specific gravity is measuring the [] of solutes in the urine

**Serum osmolality > 290 mOsm/L
Treatment:
1) Adequate fluid intake.

2) For CENTRAL DI:
=Intranasal desmopression (=ADH analog)

3) For NEPHROGENIC DI:
=Hydrochlorothiazide
=Indomethacin
=Amiloride
What is SIADH?
**Syndrome of inappropriate ADH secretion:
1) Excessive water retention
2) Hyponatremia
3) Urine osmolarity > serum osmolarity
Causes of SIADH:
1) Ectopic ADH
= small cell lung cancer

2) CNS Disorders/head trauma

3) Pulmonary disease

4) Drugs
=ex. cyclophasphamide
Where is ADH made?
**Made in the hypothalamus --> released into the posterior pituitary
Complications:
**Very low serum sodium levels can lead to SEIZURES
=correct slowly
Treatment:
**Treat w/ demeclocycline OR H20 restriction
What is carcinoid syndrome?
=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!
Symptoms of Carcinoid Syndrome
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
Rule of 1/3's:
1/3 metastasize

1/3 present w/ 2nd malignancy

1/3 multiple
Treatment:
Octreotide
Zollinger-Ellison Syndrome
=Gastrin-secreting tumor of the pancreas OR duodenum

=Causes recurrent ulcers

**May be associated w/ MEN Type I