12 endocrine

Question 1

Pancreatitis

Answer 1

Secondary to tissue destruction caused by digestive enzymes released from damaged exocrine pancreatic cells
Acute (hemorrhagic)
Chronic

Question 2

Acute (hemorrhagic) pancreatitis

Answer 2

Necrosis caused by enzymes

Question 3

Acute pancreatitis causes

Answer 3

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)

Question 4

Most common causes of pancreatitis

Answer 4

80% due to gallstones and ETOH abuse

ETOH causes overactive enzymes and protein plugs within pancreatic ducts

Question 5

Patho of acute (hemorrhagic) pancreatits

Answer 5

Digestive enzymes cause destruction and liquefaction of digested pancreas tissue, which calcify
Massive edema, hemorrhage, necrosis

Question 6

Clinical manifestations of acute pancreatitis

Answer 6

Abdo pain/distension
N/V
Diaphoresis
Syncope
Shock

Question 7

Pancreatic enzymes inside pancreatic ducts which cause pancreatitis

Answer 7

Trypsin, peptidase, elastase, amylase, lipase

Question 8

Chronic pancreatitis definition

Answer 8

Irregular fibrosis replaces portions of pancreatic tissue

Progressive and irreversible

Question 9

Causes of chronic pancreatitis

Answer 9

ETOH HX

Trauma/surgery or endocrine disorders

Question 10

Patho of chronic pancreatitis

Answer 10

Tissue becomes fibrotic and firm, stones often form in fluid, islets of langerhans become fibrotic

Question 11

Clinical manifestations of chronic pancreatitis

Answer 11

Pain, endocrine insufficiency (decreased digestive enzymes)

Decreased insulin

Question 12

THE BEETIES

Answer 12

Syndrome causes altered carb, protein and fat metabolism characterized by hyperglycemia

Question 13

TYPE I BEETIES

Answer 13

Abrupt onset

Etiology maybe -genetic, viral, autoimmune

Question 14

Knowns of IDDM

Answer 14

Decrease in size and number of islet cells
Beta cells (insulin) destroyed
Hyperglycemia occurs at 80-90% loss

Question 15

Clinical manifestation of TYPE I BEETIES

Answer 15

Glucose spills into urine
Protein and fat break down cause weight loss
Polyuria, polydipsia, polyphagia
DKA
acetone breath
hyperG

Question 16

NIDDM

Answer 16

Not ketosis prone

Genetic

Question 17

Patho of NIDDM

Answer 17

Possibly decreased but can be normal size number beta cells

Insulin resistance

Question 18

Latest theory of NIDDM

Answer 18

chronic alterations between hyper and hypoglycemia

Question 19

Clinical manifestations of NIDDM

Answer 19

Increase glucose stimulates growth of microorganisms (nonspecific recurrent infections)
Visual changes (blood glucose alter water levels and eyes blur)
Paresthesia
Fatigue

Question 20

Gestational beeties

Answer 20

More likely in fatties
2/3rd trimester
4% of preggos

Question 21

Suspected cause of gestie beeties

Answer 21

excessive human placental lactogenic hormone

Question 22

Gestie beeties more

Answer 22

Mother's sugar but not insulin crosses placenta
Untreated can lead to fetal macrosomia
Hypoglycemia
Hyperbilirubinemia
Greater rate of c sections

Question 23

Fetal macrosomia

Answer 23

Big baby

Question 24

Beeties insipidus

Answer 24

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

Question 25

Clinical manifestions of beeties insipidus

Answer 25

Polyuria, thirst, polydipsia, large bladder capacity

Question 26

Complications of beeties

Answer 26

Hypoglycemia, DKA, hyperosmolar, hyperglycemic, nonketotic syndrome

Question 27

Hypoglycemia

Answer 27

<4mmol/L | Too much slin, not enough food, exercise, too much oral hyperglycemia agents, ETOH, salicylates

Question 28

Hypoglycemia adrenergic reaction

Answer 28

Tachy, diaphoretic, tremors, pallor, hunger, headache, irritability, confusion, dbl vision, ceaser, coma

Question 29

Patho of DKA

Answer 29

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

Question 30

Clinical manifestations of DKA

Answer 30

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

Question 31

Hyperosmolar, hyperglycemic, nonketotic syndrome

Answer 31

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

Question 32

Clinical manifestations of hyperosmolar, hyperG, nonK syndrome

Answer 32

Severe glucosura and polyuria (19g/hr glucose lost) Dehdydration Stupor

Question 33

Macrovascular (complication of chronic beeties)

Answer 33

Lesions in large arteries, pts have premature atherosclerosis, increased movement of LDL for metabolism -CAD, CVD, aortic atherosclerosis

Question 34

Microvascular - diabetic microangiopathy

Answer 34

Thickening of cap basement membrane, which decreases tissue perfusion (hypoxia, ischemia) Effects eyes and kidneys

Question 35

Retinopathy

Answer 35

Retina is the most metabolically active structure (by weight) in the body Microvascular issues cause vision loss, hemorrhage, retinal detachment

Question 36

Renal microangiopathy

Answer 36

Hyper G, hyperfiltration, increased blood viscosity, thickening of glomerular caps Glomerulus becomes hyalinized and afunctional More prone to infections als

Question 37

Diabetic neuropathy

Answer 37

Unknown cause, but multifactorial | Slowed motor and sensory nerve conduction, distal portions affected first

Question 38

Peripheral vascular disease

Answer 38

Occlusions of small arterioles cause gangrenous changes of feet and toes

Question 39

Beeties and infections

Answer 39

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

Question 40

Goiter

Answer 40

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)

Question 41

Hyperthyroidism

Answer 41

Thyrotoxicosis | Intolerance and increased tissue sensativity to stim by sympathetic nervous tissue

Question 42

Hyperthyroidism causes

Answer 42

``` Graves disease (autoimmune, antibodies bind and mimick TSH) Toxic goiter Thyroid crisis (thyroid storm) ```

Question 43

Clinical manifestations of hyper thyroid

Answer 43

Goiter (graves or toxic goiter) N/V, anorexia, sweating flushed skin, tachycardia, exophtalmoses, increased CO, dysrhythmias, restlesness, nervousness, tremors, weight loss

Question 44

Exophtalmoses

Answer 44

Bulging eyes (hyperthyroid)

Question 45

Thyroid storm

Answer 45

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,

Question 46

Hypothyroidism

Answer 46

``` Deficient production of TH by thyroid gland Hashimoto - autoimmune Myxedema Cretinism - congenital Surgery Iodine deficiency ```

Question 47

Hypothyroidism

Answer 47

In early life cretinism. Slowed growth of skeleton and nervous system, plus mentally retarded

Question 48

Hypothyroidism in adults

Answer 48

Slow heart, low basal metabolic rate, decreased cold tolerance, fatigue, weight gain, lethargy, myxedema

Question 49

Hypothyroid clinical manifestations

Answer 49

Low BMR Goiter Pale cool skin (myxedema of CT) Bradycardia, cardiomegalia, cold intolerance, lethargy, slow intellectual function, weight increase with decreased appetite