Patho Endocrine 2

42問 • 2年前

問題一覧

Made up of neurons that secrete hormones: epinephrine and norepinephrine, stimulation of the cortex by sympathetic nervous system, release of hormones into blood triggers “fight or flight”.

Adrenal Medulla

Atrophy and hypertrophy, decreased TSH, decreased response to TRH -> hypothyroidism

Effects of Aging on Thyroid

Cells replaced with fat, decreased insulin and receptors -> insulin resistance

Effects of Aging on Pancreas

Decreased secretion, muscle and bone mass, changes in reproductive and cognitive function.

Effects of Aging on GH

Decreased clearance by kidneys and liver, decreased secretion (disrupted circadian rhythm)

Effects of Aging on Cortisol

Most common thyroid disorder. Iodine deficiency. Autoimmune thyroiditis (Hashimotos and lymphocytic thyroiditis)-> inflammatory destruction of thyroid gland. Circulating autoantibodies and T-lymphocytes. Genetic predisposition. Manifestations with goiter. Postpartum thyroiditis (r/t Hashimotos onset 6-12 months post-partum). Congenital hypothyroidism-thyroid tissue is absent (results from absent thyroxine -> impaired neurologic development; screen newborn to intervene). Thyroid carcinoma (risks from ionizing radiation and euthyroid). Idopathic ablation or removal of gland.

Primary Hypothyroidism

Pituitary failure to synthesize TSH or TRH, caused by pituitary tumors, TBI, or SAH.

Secondary Hypothyroidism

Typically post-viral process that results in autoimmune injury to thyroid

Subclinical Hypothyroidism

A condition that results in elevated thyroid hormone T3 and T4, and decreased TSH

Hyperthyroidism

Autoimmune (Type II hypersensitivity). Genetic and environmental etiology. Manifestations: exophthalmous and pretibial myxedema

Graves Disease

Thyroid gland increases in size in response to increased TSH. Benign or cancerous forms. Lack exopthalmous and pretibial myxedema.

Nodular Disease

Decreased LOC r/t severe hypothyroidism. Preceding events: infection, discontinuation of thyroid meds, overuse of narcotics/sedatives. Patients with comorbidities at increased risk. Manifestations: hypothermia, hypoventilation, hypotension, hypoglycemia, lactic acidosis, coma. Treatment -> hormone replacement.

Myxedema Coma

Rare but dangerous, acute hyperthyroidism. Often occurs in individuals with hyperthyroidism that is undiagnosed or partially treated when exposed to a stressor. Sudden release of T4 and T3 that exceeds metabolic demand -> hyperthermia, tachycardia, high U/O, HF, agitation, delirium, N/V. Treatment -> thyroid blocking meds and supportive treatment (radioactive iodine, therapy, surgery).

Thyrotoxic Crisis (Thyroid Storm)

Excess aldosterone secretion by adrenal cortex (typically the result of adrenal carcinoma; secondary- dysfunction of RAS system). Manifestations: hypokalemia, insulin resistance, LV remodeling (HTN and hypervolemia)

Hyperaldosteronism

Increased cortisol; pituitary adenoma-> increased ACTH (loss of circadian rhythm of ACTH and cortisol, inability to increase ACTH in response to stress). Manifestations: weight gain from increased adipose tissue, insulin resistance, and protein wasting. “Moon Face”.

Cushing’s Syndrome

Adrenal insufficiency(decreased cortisol and aldosterone synthesis, increased ACTH). Primary type: caused my destruction of adrenal cortex (autoimmune, infection (usually viral), tumor, genetic (X-linked). Secondary type : caused by prolonged suppression of cortisol secretion (glucocorticoids).

Addison’s Disease

Group of metabolic diseases characterized by hyperglycemia resulting from: deficits in insulin secretion and/or insulin action.

HbgA1C > 6.5, fasting glucose > 126, 2-hr postprandial glucose > 200

Diagnosis of DM

Loss of Beta cells (loss of insulin production). Not typical before 6 months peak diagnosis 12 years. Type 1B: not autoimmune. Type 1A: Genetic susceptibility. Environmental factors? Alpha and Beta cells (insulin and amylin) function is abnormal to varying degrees. Excess glucagon causes hyperglycemia and hyperketonemia. Immune mediated T-cell destruction of Beta cells (lymphocytes and marcophages infiltrate and destroy islet cells). Reponse to a virus?

DM Type 1

Not autoimmune, “secondary”

DM Type 1B

DM Type 1A

is autoimmune

Genetic and environmental Interaction. Risk factors: obesity, age, HTN, inactivity and family history. Metabolic syndrome: increased waist circumference, elevated TG, low HDL, HTN, fasting glucose > 100

DM Type 2

Decreased insulin secretion -> insulin resistance (tissues fail to respond to insulin related to insulin molecule abnormalities, insulin antagonists, down-regulated receptors, altered glucose transport proteins, decreased activation post-receptor kinase)

Pathophysiology of DM Type 2

Regulates food intake, body mass, and reproductive function. Also, found in high levels in obese patients

Leptin

Affects several metabolic processes and is mainly known for 2 functions: insulin-sensitizing and anti-inflammatory effects. Lower-than-normal levels in T2DM-> metabolic syndrome

Adiponectin

Differences between leptin and adiponectin

Leptin enhances metabolism and reduces appetite. Adiponectin increases insulin sensitization and is anti-inflammatory. Abnormal levels of both leptin and adiponectin are associated with obesity. However, while higher body fat results in elevated leptin, it lowers adiponectin levels.

_____ are produced by white adipose tissue and obesity changes levels decreasing insulin synthesis and increasing insulin resistance.

Adipokines (increased leptin and decreased adiponectin)

Elevated free fatty acids increase ____ and _____ and cause intracellular insulin signaling, _____ tissue response to insulin , and pro-inflammatory.

TG and cholesterol; decreased

Obesity causes release of inflammatory _____, and induces insulin resistance and contributes to ____, _____, and _____.

cytokines; fatty liver, dyslipidemia, and atherosclerosis

Alterations in oxidative phosphorylation in cellular mitochondria cause _____ and changes in cellular metabolism.

insulin resistance

Obesity associated with _____ and _____.

hyperinsulinemia and decreased insulin receptors

Beta cell dysfunction (decrease in weight and number). Glucagon increases (pancreatic Alpha cells less responsive to glucose inhibition cause increased gluconeogenesis and glycogenolysis). Amylin decreases (loss of satiety and increased glucagon production). GI hormones (ghrelin and incretins) decrease insulin response to meal and increase insulin resistance.

Pathophysiology of DM II

Acute Complications of Diabetic Ketoacidosis Arise From?

Hyperglycemia and Hypoglycemia

Glucose <47 in first 48 hrs of life of <70 in children and adults. Causes: Exogenous (meds, alcohol, exercise); Endogenous (tumors of pancreas, inherited disorders); Functions (hyperalimentation, liver disease). Manifestations: AMS, tachycardia, palpitations, diaphoresis, tremors.

Acute Complications of Hypoglycemia

Oxidative stress->ROS. Polyol Pathways (Alternative pathway for glucose metabolism when activated sorbitol (intracellular osmotic pressure + glutathione (oxidative injury in blood vessels). Protein Kinase C causes insulin resistance, cytokine production, angiogenesis and microvascular changes. Glycation - glucose binds irreversibly to collagen, proteins in RBC, vessel walls and interstitum have advanced glycation end products with abnormal cell proliferation and inflammatory changes.

Chronic DM Complications

Damage to vessels, vasoconstriction, platelet aggregation, hypoxemia. Thickening of retinal capillary and increased membrane permeability with vein dilation and microaneurysm formation. Retinal ischemia with areas of poor perfusion and infarcts. Angiogenesis and fibrous tissue formation in the retina or optic disc. Increased risk of macular edema, glaucoma, and cataracts.

Retinopathy Related to DM

Hyperglycemia-> polyol pathway, protein kinase C and inflammation-> advanced glycation end products. Renal glomerular changes (glomerular enlargement and basement membrane thickening; diffuse nodular glomerulosclerosis-> loss of podocytes, decreased GFR)

Nephropathy Related to DM

Etiology- metabolic and vascular changes related to chronic hyperglycemia (inflammation, ischemia, oxidative stress, advanced glycation end products, increased polyols-> demyelination, nerve degeneration, delayed conduction). Starts in Schwann cell degeneration in peripheral sensory nerves -> can include spinal cord and posterior root ganglia degeneration.

Neuropathy Related to DM

Etiology - impaired tissue oxygen, high glucose levels, impaired immune responses, decreased sensation, delayed healing

Infection Related to DM

HTN, DMI associated with microalbuminuria, DM2 metabolic syndromes. Increased risk for CAD and stroke. MI more deadly in DM patients.

CV Disease Related to DM

Ischemic and lacunar strokes risk increased r/t autonomic nervous system. Neuropathy associated Afib and platelet coagulopathy.

Stroke Related to DM

Atherosclerosis of LE with increased risk for ulcers, gangrene, and BTK amputation

PVD Related to DM

Patho Renal

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