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Pathology > 12 endocrine > Flashcards

12 endocrine Flashcards

1
Q

Pancreatitis

A

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

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2
Q

Acute (hemorrhagic) pancreatitis

A

Necrosis caused by enzymes

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3
Q

Acute pancreatitis causes

A

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)

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4
Q

Most common causes of pancreatitis

A

80% due to gallstones and ETOH abuse

ETOH causes overactive enzymes and protein plugs within pancreatic ducts

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5
Q

Patho of acute (hemorrhagic) pancreatits

A

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

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6
Q

Clinical manifestations of acute pancreatitis

A 
Abdo pain/distension
N/V
Diaphoresis
Syncope
Shock
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7
Q

Pancreatic enzymes inside pancreatic ducts which cause pancreatitis

A

Trypsin, peptidase, elastase, amylase, lipase

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8
Q

Chronic pancreatitis definition

A

Irregular fibrosis replaces portions of pancreatic tissue

Progressive and irreversible

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9
Q

Causes of chronic pancreatitis

A

ETOH HX

Trauma/surgery or endocrine disorders

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10
Q

Patho of chronic pancreatitis

A

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

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11
Q

Clinical manifestations of chronic pancreatitis

A

Pain, endocrine insufficiency (decreased digestive enzymes)

Decreased insulin

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12
Q

THE BEETIES

A

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

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13
Q

TYPE I BEETIES

A

Abrupt onset

Etiology maybe -genetic, viral, autoimmune

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14
Q

Knowns of IDDM

A

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

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15
Q

Clinical manifestation of TYPE I BEETIES

A 
Glucose spills into urine
Protein and fat break down cause weight loss
Polyuria, polydipsia, polyphagia
DKA
acetone breath
hyperG
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16
Q

NIDDM

A

Not ketosis prone

Genetic

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17
Q

Patho of NIDDM

A

Possibly decreased but can be normal size number beta cells

Insulin resistance

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18
Q

Latest theory of NIDDM

A

chronic alterations between hyper and hypoglycemia

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19
Q

Clinical manifestations of NIDDM

A

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

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20
Q

Gestational beeties

A

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

21
Q

Suspected cause of gestie beeties

A

excessive human placental lactogenic hormone

22
Q

Gestie beeties more

A 
Mother's sugar but not insulin crosses placenta
Untreated can lead to fetal macrosomia
Hypoglycemia
Hyperbilirubinemia
Greater rate of c sections
23
Q

Fetal macrosomia

A

Big baby

24
Q

Beeties insipidus

A

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

25
Q

Clinical manifestions of beeties insipidus

A

Polyuria, thirst, polydipsia, large bladder capacity

26
Q

Complications of beeties

A

Hypoglycemia, DKA, hyperosmolar, hyperglycemic, nonketotic syndrome

27
Q

Hypoglycemia

A

<4mmol/L

Too much slin, not enough food, exercise, too much oral hyperglycemia agents, ETOH, salicylates

28
Q

Hypoglycemia adrenergic reaction

A

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

29
Q

Patho of DKA

A

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

30
Q

Clinical manifestations of DKA

A

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

31
Q

Hyperosmolar, hyperglycemic, nonketotic syndrome

A

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

32
Q

Clinical manifestations of hyperosmolar, hyperG, nonK syndrome

A

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

33
Q

Macrovascular (complication of chronic beeties)

A

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

34
Q

Microvascular - diabetic microangiopathy

A

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

35
Q

Retinopathy

A

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

36
Q

Renal microangiopathy

A

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

37
Q

Diabetic neuropathy

A

Unknown cause, but multifactorial

Slowed motor and sensory nerve conduction, distal portions affected first

38
Q

Peripheral vascular disease

A

Occlusions of small arterioles cause gangrenous changes of feet and toes

39
Q

Beeties and infections

A

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

40
Q

Goiter

A

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)

41
Q

Hyperthyroidism

A

Thyrotoxicosis

Intolerance and increased tissue sensativity to stim by sympathetic nervous tissue

42
Q

Hyperthyroidism causes

A 
Graves disease (autoimmune, antibodies bind and mimick TSH)
Toxic goiter
Thyroid crisis (thyroid storm)
43
Q

Clinical manifestations of hyper thyroid

A

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

44
Q

Exophtalmoses

A

Bulging eyes (hyperthyroid)

45
Q

Thyroid storm

A

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,

46
Q

Hypothyroidism

A 
Deficient production of TH by thyroid gland
Hashimoto - autoimmune
Myxedema
Cretinism - congenital
Surgery
Iodine deficiency
47
Q

Hypothyroidism

A

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

48
Q

Hypothyroidism in adults

A

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

49
Q

Hypothyroid clinical manifestations

A

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

Pathology (24 decks)

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