12 endocrine Flashcards
Pancreatitis
Secondary to tissue destruction caused by digestive enzymes released from damaged exocrine pancreatic cells
Acute (hemorrhagic)
Chronic
Acute (hemorrhagic) pancreatitis
Necrosis caused by enzymes
Acute pancreatitis causes
Obstruction of main pancreatic duct (gallstones)
Disruption of acinar cells (trauma)
Chemical injury (drugs)
Infection (coxsackie b, cytomegalovirus, mumps)
Overstim of acinar cells (fatty foods, ETOH)
Most common causes of pancreatitis
80% due to gallstones and ETOH abuse
ETOH causes overactive enzymes and protein plugs within pancreatic ducts
Patho of acute (hemorrhagic) pancreatits
Digestive enzymes cause destruction and liquefaction of digested pancreas tissue, which calcify
Massive edema, hemorrhage, necrosis
Clinical manifestations of acute pancreatitis
Abdo pain/distension N/V Diaphoresis Syncope Shock
Pancreatic enzymes inside pancreatic ducts which cause pancreatitis
Trypsin, peptidase, elastase, amylase, lipase
Chronic pancreatitis definition
Irregular fibrosis replaces portions of pancreatic tissue
Progressive and irreversible
Causes of chronic pancreatitis
ETOH HX
Trauma/surgery or endocrine disorders
Patho of chronic pancreatitis
Tissue becomes fibrotic and firm, stones often form in fluid, islets of langerhans become fibrotic
Clinical manifestations of chronic pancreatitis
Pain, endocrine insufficiency (decreased digestive enzymes)
Decreased insulin
THE BEETIES
Syndrome causes altered carb, protein and fat metabolism characterized by hyperglycemia
TYPE I BEETIES
Abrupt onset
Etiology maybe -genetic, viral, autoimmune
Knowns of IDDM
Decrease in size and number of islet cells
Beta cells (insulin) destroyed
Hyperglycemia occurs at 80-90% loss
Clinical manifestation of TYPE I BEETIES
Glucose spills into urine Protein and fat break down cause weight loss Polyuria, polydipsia, polyphagia DKA acetone breath hyperG
NIDDM
Not ketosis prone
Genetic
Patho of NIDDM
Possibly decreased but can be normal size number beta cells
Insulin resistance
Latest theory of NIDDM
chronic alterations between hyper and hypoglycemia
Clinical manifestations of NIDDM
Increase glucose stimulates growth of microorganisms (nonspecific recurrent infections)
Visual changes (blood glucose alter water levels and eyes blur)
Paresthesia
Fatigue
Gestational beeties
More likely in fatties
2/3rd trimester
4% of preggos
Suspected cause of gestie beeties
excessive human placental lactogenic hormone
Gestie beeties more
Mother's sugar but not insulin crosses placenta Untreated can lead to fetal macrosomia Hypoglycemia Hyperbilirubinemia Greater rate of c sections
Fetal macrosomia
Big baby
Beeties insipidus
Insufficiency of ADH leading to polyuria and polydipsia
Unable to concentrate urine leading to an increase in plasma osmolality, stimulates thirst
Called beeties cuz polyuria
Clinical manifestions of beeties insipidus
Polyuria, thirst, polydipsia, large bladder capacity
Complications of beeties
Hypoglycemia, DKA, hyperosmolar, hyperglycemic, nonketotic syndrome
Hypoglycemia
<4mmol/L
Too much slin, not enough food, exercise, too much oral hyperglycemia agents, ETOH, salicylates
Hypoglycemia adrenergic reaction
Tachy, diaphoretic, tremors, pallor, hunger, headache, irritability, confusion, dbl vision, ceaser, coma
Patho of DKA
Lipolysis for fuel, increased free fatty acids in blood, oxidized into ketones
Alterered metabolism builds of lactic acid
Degradation of amino acids means protein wasting, weakness, organ dysfunction
Clinical manifestations of DKA
Polyuria and dehydration, glucose in urine means osmotic diuresis, metabolic acidosis (ketoacids bind with bicarb) hyper K, hyper Na+ and kussmal resps, postural hypotension, CNS depression, N, abdo pain, thirst, acetone breath
Hyperosmolar, hyperglycemic, nonketotic syndrome
Same patho as DKA, lower levels of FFA and no ketosis because some insulin is present (enough to prevent lipolysis)
Usually from recent illness (often an infection) limits fluid intake and causes dehydration
Pts experience severe hypergylcemia (>33.3) which creates osmotic diuresis and further dehydration
Clinical manifestations of hyperosmolar, hyperG, nonK syndrome
Severe glucosura and polyuria (19g/hr glucose lost)
Dehdydration
Stupor
Macrovascular (complication of chronic beeties)
Lesions in large arteries, pts have premature atherosclerosis, increased movement of LDL for metabolism
-CAD, CVD, aortic atherosclerosis
Microvascular - diabetic microangiopathy
Thickening of cap basement membrane, which decreases tissue perfusion (hypoxia, ischemia)
Effects eyes and kidneys
Retinopathy
Retina is the most metabolically active structure (by weight) in the body
Microvascular issues cause vision loss, hemorrhage, retinal detachment
Renal microangiopathy
Hyper G, hyperfiltration, increased blood viscosity, thickening of glomerular caps
Glomerulus becomes hyalinized and afunctional
More prone to infections als
Diabetic neuropathy
Unknown cause, but multifactorial
Slowed motor and sensory nerve conduction, distal portions affected first
Peripheral vascular disease
Occlusions of small arterioles cause gangrenous changes of feet and toes
Beeties and infections
Decreased sensory makes pts more prone to tissue injuries
Pathogens thrive in high glucose environment
Peripheral vascular hypoxia decreases defense mechanisms
WBC function is impaired
Goiter
Enlargement of thyroid gland (from hypo or hyper thy)
Causes can be iodine deficiency
Toxic goiter (over stimulation by TSH)
Goitrogens (cabbage, turnips, lithium, fluoride)
Hyperthyroidism
Thyrotoxicosis
Intolerance and increased tissue sensativity to stim by sympathetic nervous tissue
Hyperthyroidism causes
Graves disease (autoimmune, antibodies bind and mimick TSH) Toxic goiter Thyroid crisis (thyroid storm)
Clinical manifestations of hyper thyroid
Goiter (graves or toxic goiter)
N/V, anorexia, sweating flushed skin, tachycardia, exophtalmoses, increased CO, dysrhythmias, restlesness, nervousness, tremors, weight loss
Exophtalmoses
Bulging eyes (hyperthyroid)
Thyroid storm
Can die in 48 hours, most common in undiagnosed or partially treated severe hyperthyroid, and subjected to excessive stress like infection, pulmonary or cardio disorders, emotional, dialysis, plasmaphersis,
Hypothyroidism
Deficient production of TH by thyroid gland Hashimoto - autoimmune Myxedema Cretinism - congenital Surgery Iodine deficiency
Hypothyroidism
In early life cretinism. Slowed growth of skeleton and nervous system, plus mentally retarded
Hypothyroidism in adults
Slow heart, low basal metabolic rate, decreased cold tolerance, fatigue, weight gain, lethargy, myxedema
Hypothyroid clinical manifestations
Low BMR
Goiter
Pale cool skin (myxedema of CT)
Bradycardia, cardiomegalia, cold intolerance, lethargy, slow intellectual function, weight increase with decreased appetite
