Endocrine Pathology

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Created by:

hodgeske  on March 2, 2011

Classes:

LC DPT 2013

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Endocrine Pathology

Endocrine Communication
Endocrine cell->
Chemical messenger->
Bind receptor on target cell(autocrine,paracrine or endocrine)->
Effect
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Endocrine Communication Endocrine cell->
Chemical messenger->
Bind receptor on target cell(autocrine,paracrine or endocrine)->
Effect
Endocrine System in stress Increase Energy
Increase Blood flow
Immune function
Anterior Pituitary Pathology Usually Tumor related
Gigantism - children cause excessive growth of long bones
Acromegally- adults- thickening of bones (face, jaw, hands) and hypertrophy of soft tissue)
Anterior Pituitary Pathology Usually Tumor Related
Increase ACTH= Cushings disease
Hyperpituitarism- Increased prolactin, TSH or FSH
Hypopitutiarism (rare)- decrease ant. pit hormones (GH=short, ACTH=addison's, TSH=hypothyroidism)
Anterior Pituitary Clinal Implications Arthritis
Muscle weakness
Changes in joint mobility
Thicening of intervertebral disks-> back pain
Posterior Pituitary- Diabetes Insipidus Deficiency ADH
Na resorption, Water follows-> polyuria, dehydration
Posterior Pituitary-Syndrome Inappropriate Antidiuretic Hormone (SIADH) Secretion ADH excess (Tumor, infection, trauma, over med)
Water retention- Na excretion-> hypernatermia-> lethargy, nausea, anorexia
Water intoxication- cells swell
Thyroid- Grave's Disease doesn't kill Thyroid cells- autoimmune- enlargement and secrete TH
GOITER, Increased metabolism, THYROID STORM- fever, tachycardia, delirium, irritability brought on by stress
Thyroid-Hypothyroiditis -NO Active T3/T4, autoimmunte, iodine deficiency
-SLOW Metabolism, bradycardia, decreases GIT function, Increase cholesterol->athroslerosis-> heart disease
-myxedema- separation of CT in eyes, hand, feet
-Viscous edema- spongy edema and not lymphedema- UE Problems- weakness- PSEUDOGOUT
Hypothyroditis Clinical Implications Joint mobility issues, muscle weakness, CV weakness, Activity intolerance
Grave's Disease Clinical Implications CV weaknes, heat intol, periarthritis, frozen shoulder, prox. muscle weakness
Thyroid Pathology Goiter- enlargement thyroid gland- hyper/hypo thyroidism, iodine deficiency
Thyroiditis-def TH, autoimmune, dysphagia
Thyroid Cancer-palpate nodules
Parathyroid-Hyperparathyroidism Excess PTH, usually tumor, hypocalcemia
Bone damage, kidney damage-> problems with other systems
Clinical Imps: weak bones, muscle weakness and atrophy, polyarthriis from CPPD
Parathyroid- hypoparathyroidism Def PTH, accidental remove PT, or inadequate blood supply
hypocalcemia
Clinical Implications: tetany, fall prevention, avoid hyperventilation, heart complications, cognitive deficit(memory, concentration, mood swings
Adrenal- Conn's Syndrome Increased Aldosterone and K+
Tumor, renal hypertension
Hypernatremia(excess Na)-> hypervolemia-> increased BP-> heart failure
Clinical Imp: tetany, cardia disryhthmia, paresthesia, muscle weakness
Adrenal-Addison's Disease Decreased Cortisol and aldosterone- autoimmune
glucocorticoid def.- can't combat stress
causes Weakness, exhaustion, hypotension and Increased ACTH and MSH (BRONZE SKIN)
Aldosterone def cause increase Na exretion-> water loss etc to cardiac failure
Increased K+ retention-> heart attack
Addison disease - clinical implication minimize stress (no thermal pool)
addison crisis: dizziness, nausea, profuse sweating, increases HR, tremor
look for signs of infection or illness
Hypocortisolism Cortisol treatment, remove exogenous source abruptly, system can't deal and down regulate ant. pit and adrenal cortex
Pancreas- Type I Diabetes Insulin dependent and deficient
autoimmune loss of Beta cells
Hyperglycemia, ketoacidosis, damage eyes, kidneys, nerves, hear and blood vessels
Use exogenous insulin to control
Pancreas- Type II Diabetes noninsulin dependent and insulin resistanct
risk factors are obesity, sesentary, smoking, age
Hyperglycemia, ketoacidosis, damage eyes, kidneys, nerves, hear and blood vessles
control with diest, exercise and oral hypoglycemic agents
Prediabetes Incomplete function: glucose uptake in reponse to insulin
decrease insulin sensitivity and increase insulin resistance
hyperglycemia, HTN, dysliidemia-> heart disease
Impaired glucose tolerance and fasting glucose
Pathology of Type I & II Diabetes Decrease glucose utilization
Increased fat mobilization
increased lipid levels
decreased protein utilization
cardiovascular-> athrosclerosis, cap occlusion, heart attack without pain
3 polys: polydisia, plyuria, polyphagia
I & II Diabetes Musculoskeletal Pathology Stiff hand syndrome
flexor tenosynovitis
adhesive ccapsulitis (sleep on wrong and wake up total stiff)
Skin scleroderma
Tendinopathy
osteoporosis
diffuse io0ipathic hyperostosis
I & II Diabetes Neuropathy Pathology Affect CNS, PNS
Sensory polyneruopahty of hand and feet- joint trauma, ulcers
Autonomic neuropathy- affect blood flow
Motor neuropathy
Diabetes Implications Impaired muscle-> weakness
amputation
neuropathy-> sensation, cognition, muscle weakness
DV and pulmonary disorder(stamina)
Integumentary-> skin compromised, wounding, slow to heal
Low glucose
Hypoglycemia- If overmedicate- can go into coma
Cushing's Disease Increase Cortisol from increase ACTH
tumor of ant. pit
Cushing's Syndrome Increase cortisol from adrenal or medication
Tumor ant pit
Cushing's disease and syndrome effects and implications Hyperglycemia, HTN, proximal muscle weakening, protuberant abdomen with purple stria, buffalo hump
IMMUNE SUPPRESSION
Clinical Imp: poor wound healing, thinning skin
Generalized muscle weakness
osteoporosis

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