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Alle Oberthemen / Medicine / Endocrinology

Cushing's Disease (39 Karten)

Sag Danke
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What's the primary problem with Cushings SYNDROME?
Glucocorticoid excess. (May or may not involve mineralcorticoid excess)

Exogenous (Most common)
Iatrogenic (given as medications)

Endogenous (Rare)
* ACTH Dependent -
-Pituitary = Cushing's Disease
-Ectopic source of ACTH

* ACTH-independent
Problem withe adrenals incorrectly producing too much Glucocorticoid
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AI
How much of the population has it?
3%
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There are 3 things that can happen in response to antigen exposure
Immune Response - Lymphocytes are activated
Immunologic Tolerance - Lymphocytes functionally inactivated
Ignorance - Lymphocytes do not react
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What's the difference between central tolerance and peripheral tolerance?
Central Tolerance:
Developing Lymphocytes are filtered out (bone marrow for B cells, Thymus for T cells)


Periphreal Tolerance
Mature lymphocytes -> Induced to be anergic
Regulatory T cells
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T2 Autoimmune diseases
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Mechanisms that induce self-tolerance
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What are the 3 kinds of hypersensitivity that are associated with Autoimmune Diseases?
Type II, III and IV.

Only Type 1 is not.

Type 2: Antibodies against cell surfaces / ECm
Type 3: Immune complexes
Type 4: Effector T cells
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AI diseases associated with III and IV hypersensitivity
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AI Diseases of the endocrine gland
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What are the Type II hypersensitivity AI diseases? What's the pathogenesis?
AI Hemolytic Anemia
IgG and IgM against RH antibodies on RBCs.
=> Complement activation & Enhanced phagocytosis
3 methods of destruction:
1) FcR+ on macrophages => Destruction
2) Binds comlement=> recruits Macrophages=>Destruction
3) Binds complement=> Complement mediated Lysis




Goodpasture's Sydnrome
IgG targets Type IV Collagen.
Antibody deposits => Kidney problems.
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What are the TIII Hypersensitivity AI diseases?
SLE: Immune complexes deposited in
1) Blood capillaries
2) Renal Glomeruli
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what are the Type IV AI diseases?
Use Effector T cells:

Pancreas: T1DM
Joints: Rheumatoid Arthritis
Brain: MS
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AI disease we should know (10 of them). The autoantigen, and the pathology
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What are the Thyroid AI diseases? What kind of Hypersensitivity?
Grave's Disease: Hyperthyroidism. Ab activates. Heat intolerance, nervousness, weight loss, BULGING EYES

Baby can get. Pregnant mother needs Plasmaphoresis to remove Ab.

Hashimoto's Disease: Hypothyroidism. Ab destroys. Germinal center generation => Goiter.
Middle Aged women common
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Myasthenia Gravis:
What's the target?
Symptoms?
Acetylcholine receptor.

Get drooping eyes, double vision.

Binding of Ab causes internalization of AChR. which reduces total number of AChR.
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What is SLE? When is it triggered? What's the main problem with SLE?
Intense inflammation
TIII hypersensitivity
Formation of immune responses in resonse to DNA, histones, ribosomes. This often happens after viral infection


Glomerulonephritis is a big problem because of kidney damage from the immune complexes

90% have arthritis.
Butterfly shaped skin rash


10:1 female to male
1:700 in women
1:250 among women of African or Asian descent.
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Rheumatoid Arthritis:
What are the effectors that mediate the disease? How frequent.? What is Rheumatoid Factor?
Effectors:
T cells, B cells, Macrophages & Neutrophils

Prostaglandins / Leukotrienes mediate inflammation


Lysosomal enzymes, proteinases, collagenases, TNF, IL-1, 8.

1-3% of the US.


80% have Anti-Antibodies called rheumatoid factor
Fc portion of human IgG
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MS
How common? What is the target & what kind of immune response causes it?

What are the main effector cells, and their effector molecules?

What are the 2 categories of MS?
Main cause of neurological disability in young people
20-30 yo onset


Inflammation of CNS White Matter (myelinated)
Involves T-cell and macrophage => Axonal injury

CD4+ T cells secrete proinflammatory cytokines (TNF- and IFN-)

Relapse-remitting (RR) - cycle between acute attack and recover. Can accumulate damage

Progressive (PP) - getting worse
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What are 2 autoimmune factors that have strong genetic factors?
MS and IDDM.

From Twin studies.
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What are the AI diseases that are more common in women? What are the AI diseases that are not?
Diseases not associated:
Goodpasteur's Sydnrome
MG
IDDM
Rheumatoid Arthritis 3


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What is the difference between Cushing's Disease and Cushing's SYNDROME?
Cushing's Disease involves a problem with the pituitaries producing too much ACTH, resulting in excess glucocorticoid

Cushing's SYNDROME involves the production of too much glucocorticoid, regardless of etiology
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In Steroid synthesis, what is the common precursor? What are the 3 broad categories of end products?
Cholesterol => Pregnenelone

Ultimate products are

Mineralcorticoids (ie Aldosterone)
Glucocorticoids (ie Cortisol)
Androgens (ie Estradiol)
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Are cortisol levels high or low first thing in the morning?
high
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What is the basic categorization for Cushing's Syndrome?
Exogenous Endogenous
Iatrogenic ACTH-dependent
ACTH-Independent
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ACTH-dependent vs. ACTH-Independent (if Endogenous)
ACTH-dependent ACTH-independent
Pituitary Dependent Iatrogenic/ Factitious
Ectopic ACTH Pigmented micronodular adrenal hyperplasia
Exogenous ACTH Adrenal hyperplasia b/c of abnormal hormone receptor function


* Macronodular adrenal hyperplasia can be both
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Differential for ENDOgenous CS
ACTH Dependent:
2/3 are Cushings: 8:1 female/male. Gradual onset. 20-40 yo. Adenoma small / occult

1/6 Ectopic ACTH/CRH: 1:3 female/male. Oat cell carcinoma. Neuroendocrine tumors that might have somatostatin receptors

ACTH-Independent
1/6 are Adrenal (ACTH Independent): NO ANDROGEN EXCESS. Autoimmune / ectopic receptor / benign or malignant growth
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What are the lab tests of the HPA axis?
1) Plasma ACTH: Sensitive
2) Plasma Cortisol: bound + free cortisol
3) Urine free cortisol: don't use this. Multiple false neg/pos
4) Salivary Cortisol: free cortisol, easy test


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Urinary free cortisol


CS will have elevated levels of free cortisol in the urine
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Plasma ACTH
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Screening vs. Confirmatory Diagnosis
1) Screening
- Overnight dexamethasone
- 24hr urine free cortisol


2) Confirmatory
- 2day Dexamethasone suppression test (DM is a synthetic glucocorticoid
- Dexamethasone-oCRH test
- Midnight salivary cortisol
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Dexamethasone Suppression


In the presence of dexamethasone, should get diminished free cortisol over a 4 day (?) period.
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Human CRH test


Should be a stimulation test to see if you can increase the Cortisol levels.
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Algorithm to identify etiology of CS - 1


1) ACTH
2) MRI- PIT
3) Bilateral Petrosal Sinus sampling for ACTH with oCRH
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Treatment options for CS
Pituitary: transsphenoidal microsurgery
Ectopic: adrenal enzyme blockers

For all of them: Rads, Medical, Bilateral adrenalectomy
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Adrenal Meds
Metyrapone
Ketoconazole
Aminoglutethimide
Mitotane
Etomidate


Neuromodulatory agents
- 5HT antagonists [ Cyproheptadine, Rianserin ]

Dopamine antagonists [Bromocriptine]
Somatostatin Analogues  [Octreotide]
GABA agonist - [Sodium Valproate]
Glucocorticoid Antagonist - [Mifepristone RU486]
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What are the effects of Glucocorticoids by tissue?
Metabolism Liver, Fat, Muscle Increased Glucose, Lipolysis, Muscle wasting
Calcium Kidney, bone, GI Reduced absorption, collagen synthesis
Immune Cells Inhibited
Skin Antiproliferative causes easy bruising
Breast Epithelium Galactorrhea
CV system / Kidney Heart, Vasculature, Kidney Increased ECF, Contractility, Response to Constrictors
Psychiatric Mood, Sleep Mood variable. Less REM, Increased Appetite
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What is 11HSD-1 and 11HSD-2?
11HSD-1 converts CORTISONE to CORTISOL, which can be used on a glucocorticoid receptor.

11HSD-2 converts CORTISOL to CORTISONE, which doesn't interact with mineralcorticoid receptors (ie in the kidney)


11HSD2 is found in kidneys and other tissues with mineralcorticoid activity

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What are the symptoms that Cushing's Shares with Metabolic Syndrome X? What are the things that are found in Cushings, but not Metabolic Syndrome X
Shared Cushing's Only
Abdominal Obesity Osteoporosis
Insulin Resistance Myopathy
Hypertension Neuropyschiatric Syndromes
Glucose Intolerance
PCOS/ hyperandrogenism
Oligomenorrhea


* Polycystic ovary disease
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In ACTH-dependent Cushing's syndrome,what does the distribution of basal cortisol look like? In Cushing's DISEASE? What's the significance?
Kartensatzinfo:
Autor: yaoyu
Oberthema: Medicine
Thema: Endocrinology
Veröffentlicht: 10.02.2010
 
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