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Endocrine II midterm > Guerin: Endocrine Pancreas > Flashcards

Guerin: Endocrine Pancreas Flashcards

1
Q

What kinds of cells are int he Islets of Langerhans?

A
  • B cells: Insulin
  • a cells: glucagon
  • d cells: somatostatin
  • PP cells: pancreatic polypeptide
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2
Q

What is somatostatin’s effect on insulin and glucagon?

A

-suppresses both of them

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3
Q

What are the rare cell types of the Islets of Langerhans?

A
  • D1 cells: Vasoactive intestinal polypeptide (VIP)

- Enterochromaffin cells: serotonin

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4
Q

what does VIP do?

A
  • induces glycogenolysis and hyperglycemia

- stimulates GI fluid secretion and causes secretory diarrhea

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5
Q

What does serotonin cause when it presents as a tumor?

A

-carcinoid syndrome

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6
Q

If someone has a fasting glucose done, where is that glucose coming from?

A

the liver

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7
Q

After a meal, what happens to insulin and glucagon levels?

A

-insulin levels rise and glucagon levels fall

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8
Q

Insulin

A
  • B cells
  • Precursor ptn is cleaved in golgi
  • C-peptide is secreted in equimolar amounts with it
  • stored in secretory granules
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9
Q

what lab do we look at to see if the B cells are working in someone who is taking exogenous insulin?

A

C peptide

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10
Q

What does the sulfonylurea recptor blokc?

A

the K+ channel…. traps K+

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11
Q

What two things does insulin decrease?

A
  • Lipolysis

- Gluconeogenesis

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12
Q

Diabetes Mellitus

A
  • hyperglycemia
  • defects in insulin secretion or action
  • damages other things if chronic
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13
Q

In the US, what is DM the leading cause of ?

A

-renal disease, adult-onset blindness, and non-traumatic lower extremity amputations

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14
Q

What is a normal glucose leve?

A

70-120

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15
Q

What is the criteria for diagnosing Diabetes?

A
  • fasting glc >126
  • random glc >200
  • 2 hour plasma glc >200 during and oral glucose tolerance test (OGTT) with a loading dose of 75 gm
  • HbA1C (glycated hemoglobin) >6.5
  • need to be repeated and confirmed on a separate visit
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16
Q

What can acute stresses like burns or trauma lead to?

A
  • transient hyperglycemia

- so, dx of Diabetes requires hyperglycemia following resolution of the acute illness

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17
Q

Impaired glucose tolerance (Prediabetes)

A
  • fasting plasma glc 100-125
  • 2 hr glc 140-199
  • HbA1C 57.-6.4%
  • up to 1/4 will develop overt diabetes over 5 years
  • also have a significant risk for CV complications
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18
Q

Which is more common, type 1 or type 2 diabetes?

A

Type 2 (90-95%)

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19
Q

Which one has the circulating islet autoantibodies?

A

DM 1

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20
Q

Which one has the diabetic ketoacidosis in absence of insulin therapy?

A

DM1

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21
Q

Which one has insulin resistance in peripheral tissues, failure of compensation by B cells?

A

-DM2

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22
Q

Which one is the one where they are fat?

A

DM2

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23
Q

Which one has insulitis (inflammatory infiltrate of T cells and macrophages)?

A

DM1

-DM2 has amyloid deposition in islets

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24
Q

Type 1 DM

A

Islet destruction is cause by immune effector cells reacting against endogenous B cell antigens
-Childhood

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25
Q

Genetic susceptibility with DM1

A
  • HLA gene cluster on Chromosome 6p21

- White ppl have HLA-DR3 or HLA-DR4 haplotype

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26
Q

Which genes have the highest inherited risk for DM1?

A

-HLAD DR3 or 4 PLUES DQ8

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27
Q

How many B cells do we have to lose to get hyperglycemia?

A

90%

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28
Q

What things do the autoantigens in DM1 target?

A
  • insulin
  • B cell enzyme glutamic acid decarboxylase (GAD)
  • Islet cell autoantigen 512 (ICA512)
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29
Q

What was the big environmental factor for DM2?

A

OBESITY!

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30
Q

Metabolic defects in DM2

A
  • insulin resistance

- inadequate insulin secretion (B-cell dysfunction)

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31
Q

Example of insulin resistance in Liver, muscle, and fat?

A
  • Liver: failure to inhibit gluconeogenesis
  • Muscle: failure of glucose uptake and glycogen synthesis after a meal
  • Fat: failure to inhibit activation of lipase…. excess triglyceride breakdown and excess circulating FFA’s
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32
Q

How are the B cells through the development of DM2?

A
  • normal
  • increased secretion of insulin
  • decreased… get tired
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33
Q

Monogenic forms of diabetes

A
  • Genetic Defects in B cell function
  • Defects that impair tissue response to insulin (IR mutations): Acanthosis nigricans and polycystic ovaries and elevated androgen levels
  • Lipatrophic diabetes: hyperglycemia with loss of adipose tissue in the subcutaneous fat
34
Q

Pregestational diabetes

A
  • when women with preexisting diabetes become preggo

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

35
Q

Gestational diabetes

A
  • woman develops impaired glucose tolerance and diabetes for the first time during preggo
  • resolves following delivery
  • if poorly controlled later in preggo, you get large newborn
36
Q

Clinical presentation of DM1

A
  • <18 y/o
  • can occur at any age tho
  • sometimes, the transition from impaired glc tolerance to overt diabetes can be abrupt…. often triggered by infection
37
Q

What is the classic triad for DM1?

A
  • polyuria, polydipsia, and polyphagia

- when severe: diabetic ketoacidosis

38
Q

Clinical presentation of DM2?

A
  • > 40 y/o
  • obese
  • noticed after routine blood testing
  • fatigue, dizziness, or blurred vision
39
Q

Diabetic Ketoacidosis

A
  • type 1 usually
  • failure to take insulin is most common trigger
  • Glc 250-600
  • hyperglycemia causes an osmotic diuresis and dehydration
40
Q

How doe diabetic ketoacidosis come about?

A
  • insulin deficiency… stimulates lipase… breakdown of adipose stores… increased FFAs
  • in the liver: FAs are esterified to fatty acyl CoA
  • in liver mitochondria: oxidatino of fatty acyl CoA molecules produces Ketone bodies!
41
Q

What happens if we also have dehydration along with diabetic ketoacidosis?

A
  • decreased urinary excretion of ketoones

- metabolic ketoacidosis

42
Q

Clinical manifestations of diabetic ketoacidosis?

A
  • Fatigue
  • Nausea and vomiting
  • Severe ab pain
  • fruity breath
  • CNS depression and coma if we don’t do anything about it
43
Q

What does reversal of ketoacidosis require?

A
  • administration of insulin
  • correction of metabolic acidosis
  • tx of the underlying precipitating factors such as infection
44
Q

Hyperosmolar hyperosmotic Syndrome (HHS) in Type 2 DM

A
  • severe dehydration resulting from sustained osmotic diuresis
  • usually only seek medical attention when: severe dehydration, imparireed mental status
  • hyperglymcemia typically 600-1200 mg/dL
45
Q

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

A
  • Hypoglycemia
  • from missing a meal or physical exertion or excess insulin administration
  • dizziness, confusion, sweating, palpitations, and tachycardia…. loss of consciousness
46
Q

How do you treat hypoglycemia?

A

-oral or IV glucose

47
Q

How do we assess glycemic control?

A
  • % of glycated hemoglobin (HbA1C)

- keep it at <7% is diabetics

48
Q

Diabetic macrovascular disease

A
  • larger to medium arteries

- accelerated atherosclerosis: increased risk of MI, stroke, and lower extremity ischemia

49
Q

Diabetic microvascular disease

A
  • small vessels

- retinal, kidneys, and peripheral nerves

50
Q

What is the hallmark for diabetic macrovascular disease?

A

-accelerated atherosclerosis involving the aorta and large and medium-sized arteries

51
Q

What is the most common cause of death in diabetics?

A

Myocardial infarction

52
Q

What do diabetics have a lot of that is an inhibitor of fibrinolysis and thus acts as a procoagulant… formation of atherosclerotic plaques

A

-PAI-1

53
Q

What is something involving the extremities that is 100 times more common in diabetics?

A

-gangrene of the lower extremities

54
Q

What blood vessel problem is more prevalent and severe in diabetics?

A

-hyaline arteriolosclerosis

55
Q

What is diabetic microangiopathy?

A
  • diffuse thickening of basement membranes

- paradoxically, diabetic capillaries are more leaky than normal to plasma proteins

56
Q

What does diabetic microangiopathy lead to ?

A

development of diabetic nephropathy, retiopathy, and some forms of neuropathy

57
Q

What is the second most common cause of death in diabetics?

A
  • Diabetic nephropathy

- Native americans, hispanics, and african americans with type 2 DM

58
Q

What is the first sign of diabetic nephropathy?

A
  • microalbuminuria… low amounts of albumin in the urine
  • if untreated…. overt nephropathy with macroalbuminuria… usually accompanied by the appearance of htn
  • end stage renal disease… dialysis or renal transplant…. more common with DM1
59
Q

What are the three lesions in diabetic nephropathy?

A
  • glomerular
  • Renal vascular lesions, principally arteriolosclerosis
  • Pyelonephritis, including necrotizing papillitis
60
Q

What happens with diabetic nephropathy to the capillary basement membrane

A
  • GBM thickening

- can only be seen by electron microscopy

61
Q

Diffuse mesangial sclerosis

A
  • mesangial increase due to thickening of GBM

- MAtrix depositions are PAS positive

62
Q

Nodular glomerulosclerosis

A
  • Kimmelstiel-Wilson disease
  • Nodules of matrix (PAS positive) situated in the periphery of the glomerulus
  • as it progresses: nodules enlarge and eventruallly obliterate the glomerular tuft
63
Q

What is that special pattern of acute pyelonephritis that is much more common in diabetics?

A

Necrotizing papillitis

64
Q

Diabetic Neuropathy

A
  • distal symmetric polyneuropathy of lower extremities is the most frequent pattern
  • upper extremities get there too…. gloce and stocking pattern of polyneuropathy
  • Autonomic neuropathy: bowel, bladder, and sometimes erectile dysfunction
  • Mononeuropathy: sudden footdrop, wristdrop, or isolated cranial nerve palsies
65
Q

What are some diabetic ocular complications?

A
  • visual impairment, sometimes even total blindness
  • 60-80% of diabetics
  • retinopathy… overexpression of VEGF in retina
  • Cataract: opacification of the lens
  • Glaucoma: increased intraocular pressure and resulting damage to the optic nerve
66
Q

In a pt with diabetic neuropathy, what could a trivial infection in the toe lead to?

A

-gangrene, bacteremia, pneumonia, even death

67
Q

If we have an insulin producing tumor in the pancreas, will it most likely be benign or malignant?

A
  • benign

- 60-90% of other functioning and nonfunctioning NETs are malignant… so insulin=good

68
Q

Genetic alterations in sporadic PanNets?

A
  • MEN1
  • LOF mutation in tumor suppressor genes: PTEN and TSC2
  • Inactivating mutations in two genes:
  • Alpha-thalassemia/mental retardation syndrome, W-linked (ATRX)
  • Death-domain associated protein (DAXX)
69
Q

What are the most common clinical syndromes in PanNETs?

A
  • hyperinsulinism
  • hypergastrinemia (ZE syndrome)
  • MEN
70
Q

Hyperinsulinism (Insulinoma)

A
  • B cell tumors
  • most common pancreatic endocrine neoplasms
  • can secrete enough insulin to induce clinically significant hypoglycemia
  • classic clinical picture: hypoglycemic episodes (if blood glucose level falls below 50 mg/dL)
  • relieved by feeding or parenteral administration of glucose
71
Q

Morphology of insulinoma

A
  • small
  • looks like giant islet cells
  • typically have deposition of amyloid
  • hyperinsulinism may also be cause by focal or diffuse hyperplasia of the islets
72
Q

What are other situations in which there is hyperplasia of the islets?

A
  • maternal diabetes (usually transient)
  • Beckwith-Wiedemann syndrome
  • Rare mutation in the B-cell K+ channel protein or sulfonylurea receptor
73
Q

Lab findings for insulinoma

A

-high circulating levels of insulin and a high insulin:glucose ratio

74
Q

Tx for insulinoma

A

surgical resection of the tumor

75
Q

Zollinger-Ellison Syndrome (gastrinomas)

A
  • marked hypersecretion of gastrin
  • as likely to arise in the duodenum and peripancreatic soft tissues as in the pancreas
  • > 50% are locally invasive or have already metastasized at the time of diagnosis
  • ~25% of pts gastrinomas arise in as part of the MEN-1 syndrome
  • histologically bland
76
Q

Clinical course of ZE syndrome?

A
  • hypergastrinemia gives rise to extreme gastric acid secretion…. peptic ulceration
  • ulcers are often unresponsive to therapy
  • can also get ulcers in unusual locations such as the jejunum
  • > 50% have diarrhea
77
Q

Tx of ZE syndrome

A
  • control of gastric acid secretion with proton pump inhibitors
  • total resection of the neoplasm, when possible, eliminates the syndrome
78
Q

What happens with pts that have ZE with hepatic metastases?

A

-progressive tumor growth leading to liver failure usually within 10 years

79
Q

alpha cell tumors (glucagonomas)

A
  • rare
  • mild DM
  • characteristic skin rash (necrolytic migratory erythema) and anemia
  • most frequently in perimenopausal and postmenopausal women
80
Q

Delta cell tumors (somatostatinomas)

A
  • DM, Cholelithiasis, steatorrhea, and hypochlorhydria
  • difficult to localize preoperatively
  • also rare
81
Q

VIPoma (release of vasoactive intestinal peptide (VIP))

A
  • rare

- watery diarrhea, hypokalemia, achlorhydria (WDHA syndrome)

82
Q

Most common Pancreatic NET?

A

-insulinoma

Endocrine II midterm (13 decks)

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