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Endocrine 2 > Endocrine pancreas > Flashcards

Endocrine pancreas Flashcards

1
Q

What are the main cell types in the islets and scattered in the exocrine pancreas and what do they secrete?

A
  • Beta: insulin
  • Alpha: glucagon
  • delta: somatostatin
  • PP: pancreatic polypeptide
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2
Q

What does glucagon do?

A

stimulates glycogenolysis in liver

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3
Q

What does somatostatin do?

A

suppresses both insulin and glucagon

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4
Q

What does pancreatic polypeptide do?

A

Stimulates secretion of gastric and intestinal enzymes and inhibits intestinal motility

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5
Q

What are the Rare cell types in the islets of Langerhans and what do they secrete

A
  • D1 cells: VIP

- Enterochromaffin cells: serotonin

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6
Q

What does VIP do?

A
  • induces glycogenolysis and hyperglycemia

- stimulates GI fluid secretion and causes secretory diarrhea

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7
Q

What is it called when there is a tumor of enterochromaffin cells secreting serotonin

A

carcinoid syndrome

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8
Q

during fasting you should have _____ levels of insulin and ______ levels of glucagon

A
  • low

- high

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9
Q

Fasting plasma glucose levels are determined primarily by what?

A

hepatic glucose output

-Hepatic gluconeogenesis and glycogenolysis

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10
Q

the insulin precursor protein is proteolytically cleaved by what?
gives what and what?

A
  • Golgi complex

- mature hormone and C-peptide

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11
Q

What can you measure in someone receiving exogenous insulin to determine how well B cells are functioning

A

C peptide levels

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12
Q

Describe the steps of insulin synthesis and secretion

A
  • Glucose comes in through GLUT-2
  • goes to mitochondria to produce ATP
  • This ATP inhibits a K+ channel on the beta cells
  • leads to membrane depolarization and influx of Ca
  • this leads to secretion of insulin
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13
Q

effects of insulin on adipose tissue

A
  • increase glucose uptake
  • increase lipogenesis
  • decrease lipolysis
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14
Q

effects of insulin on Striated muscle

A

-increase in glucose uptake, glycogen synthesis, and protein synthesis

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15
Q

effects of insulin on Liver

A
  • decrease gluconeogenesis
  • increase in glycogen synthesis
  • increase in lipogenesis
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16
Q

A group of metabolic disorders with hyperglycemia from defects in insulin secretion and/or insulin action

A

Diabetes Mellitus

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17
Q

in Diabetes mellitus, chronic hyperglycemia and metabolic dysregulation is associated with secondary damage to what?

A
  • kidneys
  • eyes
  • nerves
  • blood vessels
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18
Q

In the US, what is the leading cause of end-stage renal disease, adult-onset blindness, and non traumatic lower extremity amputations

A

Diabetes mellitus

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19
Q

What ethnic groups are more likely to develop diabetes

A
  • native americans
  • african american
  • Hispanics
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20
Q

What is normal blood glucose lever

A

70-120

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21
Q
  • Diabetes: fasting plasma glucose >/= what?
  • Random glucose level of what (in a patient with classic hyperglycemic signs)?
  • 2 hour plasma glucose of what during an oral glucose tolerance test (OGTT) with loading dose of 75 gm?
  • HbA1C (glycated hemoglobin) >/= what?
A
  • 126
  • greater than/equal to 200
  • greater than/equal to 200
  • > /= 6.5%
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22
Q

the tests for diagnosis of diabetes need to be repeated and confirmed on a separate visit except for which one?

A

the random blood glucose level in a patient with classic hyperglycemic signs

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23
Q

What acute stresses can lead to transient hyperglycemia?

A

-Severe infections, burns, trauma

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24
Q

What are the glucose levels for impaired glucose tolerance (Prediabetes)

A
  • Fasting: 100-125
  • 2 hour plasma glucose following 75 gm OGTT: 140-199
  • HbA1C: 5.7-6.4%
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25
Q

describe the progression from prediabetes to diabetes and also the cardiovascular risk

A
  • up to 1/4 of prediabetes pts will develop overt diabetes over 5 years
  • they also have significant risk for cardiovascular complications
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26
Q

2 classifications of diabetes and %’s

A
  • Type 1: 5-10%

- Type 2: 90-95%

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27
Q

This type of DM is caused by islet destruction caused primarily by immune effector cells reacting against endogenous Beta-cell antigens

A

type 1

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28
Q

Age for type 1 DM

A
  • most commonly develops in childhood and becomes manifest at puberty and progresses with age
  • can occur at any age
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29
Q

What is the MOST important locus for genetic susceptibility of type 1 DM

A

HLA gene on chromosome 6p21

  • 90-95% of caucasians with DM1 have either HLA-DR3 or DR4 haplotype
  • if DR3 or DR4 PLUS DQ8 . . . highest inherited risk
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30
Q

What are the other less important genes associated with susceptibility to DM1

A
  • Wasinsulin
  • CTLA4 and PTPN22
  • AIRE: autoimmune polyendocrine syndrome, type 1
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31
Q

clinical onset of DM1 is what?

A

abrupt

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32
Q

what % of beta cells must be lost to get hyperglycemia and ketosis

A

90%

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33
Q

What do the autoantigens target in DM1

A
  • insulin
  • Beta cell enzyme glutamic acid decarboxylase (GAD)
  • Islet cell autoantigen 512 (ICA512)
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34
Q

DM1 is failure of self tolerance in what cells?

A

T cells specific for islet antigens

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35
Q

What is the big environmental factor associated with DM2?

A

-Obesity: especially central/visceral obesity

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36
Q

What are the metabolic defects of DM2

A
  • Insulin resistance: decreased response of peripheral tissues (esp. skeletal muscle, adipose tissue, and liver) to insulin
  • Inadequate insulin secretion (Beta-cell dysfunction)
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37
Q

Inadequate insulin secretion is due to a combination of what things?

A
  • excess free fatty acids: “lipotoxicity”
  • chronic hyperglycemia: “glucotoxicity”
  • abnormal “incretin effect”
  • amyloid deposition within islets
  • genetics
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38
Q

What does insulin resistance do to liver

A
  • Failure to inhibit gluconeogenesis

- Contributes to high fasting blood glucose levels

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39
Q

What does insulin resistance do to skeletal muscles

A
  • Failure of glucose uptake and glycogen synthesis after a meal
  • contributes to high post-prandial blood glucose levels
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40
Q

What does insulin resistance do to fat

A

failure to inhibit activation of lipase –>excess triglyceride breakdown and excess circulating free fatty acids

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41
Q

What are the 2 broad categories of monogenic forms of diabetes

A
  • Genetic defects in beta cell function

- Genetic defects that impair Tissue response to insulin

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42
Q

What are the 2 monogenic forms of diabetes that impair Tissue response to Insulin?

A
  • Insulin receptor mutations: Acanthosis nigricans. Also Women frequently have polycystic ovaries and elevated androgen levels
  • Lipoatrophic diabetes: hyperglycemia along with LOSS of adipose tissue and subcutaneous fat . . also have hypertriglyceridemia, aconathosis nigricans, and fat deposition in the liver
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43
Q

Describe pregestational diabetes

What are risks

A
  • Women with preexisting diabetes become pregnant

- increased risk of stillbirth and congenital malformations in the fetus if poorly controlled

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44
Q

Describe gestational diabetes

what are risks

A
  • women develops impaired glucose tolerance and diabetes for the first time during pregnancy
  • Pregnancy is a “diabetogenic” state where the hormones favor a state of insulin resistance
  • typically resolves following delivery
  • Majority develop overt diabetes over next 10-20 years
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45
Q

What are the consequences of poorly controlled diabetes later in pregnancy

A
  • Large for gestational age newborn (macrosomia)

- child at an increased risk of developing obesity and diabetes later in life

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46
Q

DM1 classically present when?

A

<18

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47
Q

the first 1 or 2 after the onset of DM1 can be a “honeymoon period” .. describe what this is

A

-exogenous insulin requirements may be minimal because of ongoing endogenous insulin secretion

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48
Q

Sometimes, in DM1, the transition from impaired glucose tolerance to overt diabetes can be abrupt and often triggered by what?

A

an infection

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49
Q

What is the classic triad in DM1?
if severe?
also see what?

A
  • polyuria, polydipsia, and polyphagia
  • Diabetic ketoacidosis
  • weight loss and muscle weakness
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50
Q

typical age for DM2

A

> 40

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51
Q

how is DM2 usually diagnosed

A

after routine blood testing in asymptomatic persons

  • screening recommended for >45 years
  • Can present with fatigue, dizziness, or blurred vision
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52
Q

Which type of DM does diabetic ketoacidosis occur with

A

classically type 1, but can occur with type 2

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53
Q

What is diabetic ketoacidosis typically triggered by

A
  • Failure to take insulin (most common)
  • Other stressor: infections, illness, trauma and some drugs . . associated with release of epinephrine which blocks residual insulin actions and stimulates secretion of glucagon
54
Q

What are glucose levels usually in diabetic ketoacidosis

A

usually 250 to 600

55
Q

The hyperglycemia in diabetic ketoacidosis causes what?

A

-an osmotic diuresis and dehydration

56
Q

Describe the mechanism of what happens to the body in diabetic ketoacidosis?

A
  • insulin deficiency leads to activation of the ketogenic machinery
  • insulin deficiency –> stimulates lipase –> breakdown of adipose stores –> increase in free fatty acids
  • In liver: fatty acids are esterified to fatty acyl coenzyme A
  • In liver mitochondria: oxidation of fatty acyl coenzyme A molecules produces KETONE BODIES (acetoacetic acid and Beta-hydroxybutyric acid)
57
Q

When the rate of ketone body formation is greater than peripheral tissue use

A
  • ketonemia

- ketonuria

58
Q

If you get ketone body formation and also dehydration?

A

-decrease in urinary excretions of ketones –> metabolic acidosis

59
Q

Clinical manifestations of diabetic ketoacidosis

A
  • Fatigue
  • Nausea and vomiting
  • Severe abdominal pain
  • Characteristic fruity odor
  • deep, labored breathing (aka Kussmaul breathing)
  • If persists, can get CNS depression and coma (and even death)
60
Q

Reversal of Ketoacidosis requires what?

A
  • Administration of insulin
  • correction of metabolic acidosis
  • Treatment of underlying precipitating factors such as infection
61
Q

Why is it thought that ketoacidosis is lower incidence in DM2 than DM1?

A

higher portal vein insulin levels that prevent unrestricted hepatic fatty acid oxidation and keeps the formation of ketone bodies in check

62
Q

What is it called when you get severe dehydration resulting from sustained osmotic diuresis

A

Hyperosmolar hyperosmotic syndrome (HHS)

63
Q

What causes HHS and what type of DM?

A
  • in patients who do not drunk enough water to compensate for urinary losses
  • classically, pts are older and disables by a stroke or an infection
  • DM2
64
Q

HHS patients usually only seek medical attention when?

A
  • severe dehydration

- Impaired mental status

65
Q

what is the typical glucose level in HHS

A

600-1200

66
Q

What is the most common acute metabolic complication in either type of diabetes

A

Hypoglycemia

67
Q

Hypoglycemia in diabetes results from what?

A
  • missing a meal
  • excessive physical exertion
  • excess insulin administration
  • While trying to find appropriate dose of antidiabetic agents
68
Q

Signs and symptoms of hypoglycemia

A
  • Dizziness
  • confusion
  • sweating
  • palpitations
  • tachycardia
  • Eventually loss of consciousness
69
Q

What is the treatment for hypoglycemia

A

oral of IV glucose

70
Q

overwhelming majority of the morbidity and mortality of diabetes is due to what?

A

chronic complications

71
Q

Chronic diabetes takes how many years to develop

A

15-20 years after the onset of hyperglycemia

72
Q

Severity of complication of chronic diabetes is related to what

A

both degree and duration of hyperglycemia

73
Q

What are the 4 mechanisms proposed that contribute to the pathogenesis of hyperglycemia leading to chronic complications of DM

A
  • formation of advanced glycation end products (AGEs)
  • Activation of protein kinase C: vascular endothelium
  • Oxidative stress and Disturbances in polyol pathways
  • Hexosamine pathways and generation of Fructose-6-phosphate
74
Q

What provides a measure of glycemic control over the lifespan of a red cell

A

percentage of glycated hemoglobin: HbA1C

75
Q

What is the HbA1C recommended to be maintained at in diabetics

A

-<7% or even <6.5%

76
Q

normal HbA1C

A

<5.7

77
Q

What are the 2 broad categories of Chronic complications of diabetes from damage to blood vessels?
give the examples of each also

A
  • Diabetic MACROvascular disease: Large and medium sized muscular arteries. Accelerated atherosclerosis . . increased risk of MI, stroke, and lower extremity ischemia
  • Diabetic MICROvascular disease: small vessels. Retina, kidneys, and peripheral nerves
78
Q

What is the hallmark of diabetic macrovascular disease

A

Accelerated atherosclerosis involving the aorta and large and medium sized arteries
-Greater severity and earlier age of onset than non-diabetic pts

79
Q

What is the most common cause of death in diabetics

A

MI from coronary artery atherosclerosis

-followed by renal insufficiency and cerebrovascular accidents

80
Q

give me the increased risks in diabetics for macrovascular complications

A
  • 2-4 greater risk of coronary artery disease
  • 4 fold greater risk of dying from cardiovacular complication
  • increased risk also of CV in prediabetics
  • Greater risk of HTN and dyslipidemia
81
Q

Diabetics have and increase in PAI-1 . . explain what this means

A

This is an inhibitor of fibrinolysis and thus the increase acts as a procoagulant leading to formation of atherosclerotic plaques

82
Q

Gangrene of lower extremity is 100x more common in diabetics . .this is from what?

A

vascular disease

83
Q

Are larger renal arteries affected by diabetes

A

yes but microvascular damage is worse

84
Q

Describe the hyaline arteriolosclerosis associated with HTN in diabetics

A

More prevalent and more severe

85
Q

Describe diabetic microangiopathy

A
  • DIFFUSE THICKENING OF BASEMENT MEMBREANES: paradoxically the capillaries are more leaky than normal to plasma proteins
  • Most evident in capillaries of skin, skeletal muscle, retina, renal glomeruli, and renal medulla
  • Leads to development of diabetic nephropathy, retinopathy, and some forms of neuropathy
86
Q

What is the second most common cause of death in diabetics

A

diabetic nephropathy

87
Q

what is the leading caused of end stage renal disease in the US

A

diabetes

88
Q

What is he first sign of diabetic nephropathy

A

microalbuminuria: low amount of albumin in the urine (30-300 mg/day)

89
Q

Microalbuminuria is a marker for greatly increased risk for what in diabetics

A

CV morbidity and mortality

90
Q

All patients with microalbuminuria should be what?

A

screened for macrovascular disease and aggressively treated

91
Q

If untreated, 80% of type 1 and 20-40% of type 2 diabetics with microalbuminuria will develop what over 10-15 years?

A

overt nephropathy with macroalbuminuria (>300 mg of urinary albumin/day)
-usually accompanied by appearance of HTN

92
Q

> 75% of type 1 and 20% of type 2 diabetics with overt nephropathy will develops what over 20 years?

A

end stage renal disease requiring dialysis or renal transplantation

93
Q

What are the 3 lesions in Diabetic nephropathy

A
  • Glomerular lesions
  • Renal vascular lesions, principally arteriolosclerosis
  • Pyelonephritis, including necrotizing papillitis
94
Q

What are the 3 glomerular lesions in Diabetic nephropathy?

A
  • Capillary basement membrane thickening
  • diffuse mesangial sclerosis
  • nodular glomerulosclerosis
95
Q

Capillary basement membrane thickening occurs in virtually all diabetic nephropathy and can only be seen how?
begins when?
what else thickens?

A
  • electron microscopy
  • as early as 2 years after the onset of type 1 diabetes and progresses
  • tubular basement membranes
96
Q

Describe the diffuse mesangial sclerosis of diabetic nephropathy

A
  • Mesangial increase is typically associated with the overall thickening of the GBM
  • Matrix depositions are PAS positive
  • As the disease progresses it becomes nodular
  • Progresssive expansion of the mesangium correlates with measures of deteriorating renal function (e.g. proteinuria)
97
Q

Nodular glomerulosclerosis in diabetes is also called what?

A

Kemmelstiel Wilson disease

98
Q

Describe the nodular glomerulosclerosis in diabetic nephropathy

A
  • Nodules of matrix (PAS-positive) situated in the periphery of the glomerulus
  • lesions can be patchy
  • as it progresses: nodules enlarge and eventually obliterate the glomerular tuft
99
Q

In Diabetic nephropathy, you get hyalinosis of what

A

both afferent and efferent glomerular hilar arterioles

100
Q

In Diabetic nephropathy, the glomerular and arteriolar lesions lead to ischemia which then causes what?

A

tubular atrophy and interstitial fibrosis

101
Q

this is a special pattern of acute pyelonephritis that is much more common in diabetics

A

Necrotizing papillitis or papillary necrosis

102
Q

what % of diabetics have peripheral neuropathy

A
  • up to 50%

- 80% with diabetes for >15 years

103
Q

What is the most frequent pattern of involvement of diabetic neuropathy?

A

-distal symmetric polyneuropathy of lower extremity . . both motor and sensory function . .eventually upper extremities may be involved . . (“glove and stocking”)

104
Q

describe the autonomic neuropathy in diabetics

A

bowel, bladder, and sometimes erectile dysfunction

105
Q

What is the mononeuropathy in diabetics

A

sudden footdrop, wristdrop, or isolated cranial nerve palsies

106
Q

What % of diabetics have visual impairment and sometimes even total blindness

A

-60-80% 15-20 years after diagnosis

107
Q

What are the 3 visual impairments listed in diabetics?

A
  • Retinopathy from neovascularization from hypoxia-induced overexpression of VEGF in the retina
  • Cataract: opacification of the lens
  • Glaucoma: increased intraocular pressure and resulting damage to optic nerve
108
Q

Diabetics and infections

A
  • increased susceptibility to infections of the skin, tuberculosis, pneumonia, and pyelonephritis
  • Pt with diabetic neuropathy: trival infections in a toe may lead to gangrene, bacteremia, pneumonia, even death
109
Q

Pancreatic neuroendocrine tumors are tumors of what

A

pancreatic islet cells

110
Q

What is the unequivocal criteria for malignancy of pancreatic neuroendocrine tumors

A
  • metastases
  • vascular invasion
  • local infiltration
111
Q

Describe the functional status of pancreatic neuroendocrine tumors

A
  • 90% of insulin producing tumors are benign

- 60-90% of other functioning and nonfunctioning NETs are malignant

112
Q

What are the genetic alterations found in SPORADIC PanNETs

A
  • MEN1
  • loss of function: PTEN and TSC2
  • inactivationg mutations in 2 genes: Alpha-thalassemia/mental retardation syndrome, X-linked (ATRX) and Death Domain associated protein (DAXX)
113
Q

What are the most common clinical syndromes in PanNETs?

A
  • Hyperinsulinism
  • Hypergastrinemia (Zollinger-Ellison syndrome)
  • Multiple endocrine neoplasia (MEN)
114
Q

What is the momst common pancreatic endocrine neoplasm?

A

Insulinoma . . Beta cells

-Can secrete enough insulin to induce clinically significant hypoglycemia

115
Q

What is the classic clinical picture of an insulinoma

A
  • hypoglycemia episodes (if blood glucose level falls below 50)
  • confusion, stupor, and loss of consciousness
  • Precipitated by fasting or exercise
  • Relieved by feeding or parenteral administration of glucose
116
Q

Morphology of an insulinoma

A
  • usually small (often < 2 cm)
  • Histologically looks like giant islets
  • Typically have deposition of amyloid
117
Q

Besides an insulinoma, what else can cause hyperinsulinism

A

-focal or diffuse hyperplasia of the islets (previously known as nesidioblastosis)

118
Q

hyperplasia of the islets can be seen in what situations?

A
  • Maternal diabetes (usually transient)
  • Beckwith-Wiedemann syndrome
  • Rare mutations in the beta cell K+ channel protein or sulfonylurea receptor
119
Q

What % of insulinomas are symptomatic

A

20%

120
Q

lab finding in an insulinoma

A
  • high circulating levels of insulin

- high insulin to glucose ratio

121
Q

treatment of insulinoma

A

-surgical removal

122
Q

What are the other random causes of hypoglycemia mentioned

A
  • Abnormal insulin sensitivity
  • diffuse liver disease
  • inherited glycogenoses
  • ectopic production of insulin by certain retroperitoneal fibromas and fibrosarcomas
  • Induced by self injection of insulin
123
Q

What gives marked hypersecretion of gastin

A

-Gastrinomas (Zollinger-Ellison syndrome)

124
Q

Where are gastrinomas likely to arise

A

as likely to arise in the duodenum and peripancreatic soft tissues as in the pancreas

125
Q

What % of Gastrinomas are locally invasive or have already metastasized at the time of diagnosis

A

> 50%

126
Q

What % of patients with gastrinomas arise as part of MEN-1 syndrome

A

25%

127
Q

Clincal course of Zollinger-Ellison syndrome

A
  • Hypergastrinemia–>extreme gastric acid secretion –> peptic ulceration (in duodenum and stomach) . . ulcers are often unresponsive to therapy . . can also get them in jejunum
  • > 50% have diarrhea
128
Q

Treatment of Zollinger Ellison syndrome

A
  • control of gastric acid with PPI

- Total resection of neoplasm, when possible, eliminates the syndrome

129
Q

Describe the clinical course of Zollinger Ellison syndrome in those with hepatic metastases

A

progressive tumor growth leading to liver failure usually within 10 years

130
Q

Describe an alpha-cell tumor

A
  • glucagonoma
  • mild DM
  • characteristic skin rash (necrolytic migratory erythema)
  • anemia
  • Most frequently in perimenopausal and postmenopausal women
131
Q

Describe a delta cell tumor

A
  • somatostatinoma
  • DM
  • cholelithiasis
  • steatorrhea
  • hypochlorhydria
  • Difficult to localize preoperatively
132
Q

Describe a VIPoma

A
  • watery diarrhea
  • hypokalemia
  • achlorhydria (WDHA syndrome)

Endocrine 2 (10 decks)

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