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Endocrine Exam 2 > 21 - Pathology of the Thyroid II > Flashcards

21 - Pathology of the Thyroid II Flashcards

1
Q

What is diabetic MICROangiopathy?

A

A small vessel disease leading to hyaline arteriolosclerosis

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2
Q

What is the most common morphologic feature of diabetics with microangiopathy?

A
  • Diffuse thickening of basement membranes ***
  • The thickening is most evident in the capillaries of the retina and renal glomeruli

Think RETINA and KIDNEY

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3
Q

Describe the hyaline accumulation

A
  • The basal lamina separating endothelial cells from the surrounding tissue is markedly thickened by concentric layers of hyaline material composed of type IV collagen
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4
Q

Describe the properties of the capillaries

A
  • Despite the increase in the thickness of basement membranes, diabetic capillaries are MORE LEAKY than normal in terms of plasma proteins ***
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5
Q

What diabetic complications does diabetic microangiopathy lead to?

A

The microangiopathy underlies the development of

  • Diabetic nephropathy
  • Diabetic retinopathy
  • Some forms of neuropathy
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6
Q

How does diabetic microangiopathy effect a diabetic’s legs?

A

Microangiopathy worsens the ischemia caused by atherosclerosis

This is why many diabetics lose their legs ***

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7
Q

Describe the vessels of diabetic microangiopathy

A
  • High glucose leads to glycosylation
  • There is damage to the basement membrane of vessels and they become leaky
  • AGEs deposit in the wall of vessels
  • This creates a very thick membrane wall and very narrow vessels
  • This is especially harmful in the kidneys and eyes but it can happen anywhere

Thick, narrow and leak SMALL blood vessels in the capillaries of the kidneys and eyes ***

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8
Q

What are the long term complications of diabetes mellitus?

A
  • Damage to blood vessels in the kidneys
  • Damage to blood vessels in the eyes
  • Damage to nerves
  • Peripheral vascular disease
  • Coronary artery disease
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9
Q

Describe the damage to blood vessels in the kidneys

A

This can lead to…

  • Diabetic nephrosclerosis, including nodular Kimmelstiel-Wilson glomerulopathy
  • Pyelonephritis
  • Papillary necrosis
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10
Q

Describe the damage to blood vessels in the eyes

A

Exudative and proliferavitve retinopathy will occur

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11
Q

Describe the damage to nerves that will occur

A

SYMMETRIC polyneuropathy

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12
Q

Describe the diagnosis of diabetes mellitus

A
  • High fasting glucose or impaired glucose tolerance
  • Without diabetes, oral glucose loads cause only a slight rise in blood glucose due to brisk insulin response
  • With diabetes, blood glucose rises markedly for a sustained period
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13
Q

What morphological changes will you see in the kidneys of diabetic patients?

A
  • More white, which is excess basement membrane with the deposition of protein
  • This will later fibrose and hyaline structures will form
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14
Q

What is a Kimmelstiel-Wilson nodule?

A

When hyaline structures within the kidney become fibrosed

This is called diffuse glomerulosclerosis

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15
Q

What type of kidney infections are diabetic patients at risk for?

A
  • Pyelonephritis (infection of the renal pelvis)

- Cortical infections of the cortex of the kidney

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16
Q

Describe a pyelonephritis infection

A
  • Gram negative bacilli (E. coli common)
  • Causes an infection in the renal pelvis
  • The bacteria comes from the urine
  • It is a “retrograde” infection
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17
Q

Describe a cortical kidney infection

A
  • Staphylococci infection
  • Causes infection in the cortex of the kidney
  • The bacteria comes from the blood
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18
Q

What are the three types of neuropathy diabetics can experience?

A
  • Sensory
  • Peripheral
  • Visceral
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19
Q

Describe sensory neuropathy

A

Sensory neuropathy can lead to motor neuropathy - problem with myelin

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20
Q

Describe peripheral neuropathy

A
  • BILATERAL and SYMMETRIC ***
  • Progressive, irreversible
  • Parasthesia, pain, muscle atrophy
21
Q

Describe visceral neuropathy

A
  • Cranial nerve neuropathy can lead to diplopia and Bell palsy
  • GI neuropathy can lead to constipation or diarrhea
  • Cardiovascular neuropathy can lead to orthostatic hypotension
22
Q

What is diabetic MACROangiopathy?

A
  • A large vessel disease
  • A process of accelerated atherosclerosis ***
  • The problem is nonenzymatic glycosylation of lipoproteins ***
23
Q

Describe how glycosylation of lipoproteins lead to MACROangiopathy

A
  • LDLs “stick” best to glycosylated collagen
  • AGEs (advanced glycation end products) bind to their special receptors in the intima of the vessels and cause the production of fibrous tissues
24
Q

Describe the detrimental effects of MACROangiopathy

A

The result of diabetic macroangiopathy is…

  • Stroke
  • Gangrene of the lower extremities
  • Myocardia infarction ***

This will take its toll and will often occur early in life

25
Q

What can help prevent diabetic macroangiopathy?

A

Good glycemic control does help the accelerated atherosclerosis, confirming the idea that it’s due largely to the accumulation of AGEs that cause collagen production

26
Q

Describe the cause and development of neuropathic ulcers

A

Etiology

  • Peripheral sensory neuropathy
  • Trauma and deformity

Factors

  • Ischemia
  • Callus formation
  • Edema

Hard to cure - not a regular ulcer

The loss of sensation can lead to SEVERE injury since the patient doesn’t feel any pain ***

27
Q

Describe diabetic retinopathy

A
  • Ischemia due to microangiopathy and artherosclerosis serves as a stimulus for neovascular proliferation
  • These abnormally small cells are prone to hemorrhage
28
Q

What occurs in diabetic retinopathy?

A

A constellation of changes in the retina

  • Pale area of EDEMA around the central avascular macula
  • Numerous small new blood vessels at the periphery of this zone (NEOVASCULARIZATION)
  • HEMORRHAGIC FOCI
29
Q

Describe the clinical differences between type 1 and type 2 diabetes

A

Type 1

  • Onset under 20 years
  • Normal weight
  • Markedly low blood insulin
  • Anti-islet cell antibodies
  • Ketoacidosis common (DKA)

Type 2

  • Onset over 30, mostly over 40
  • Obesity ***
  • Blood insulin is normal to moderately decreased late in the disease
  • No anti-islet call antibodies
  • Ketoacidosis is rare
  • Nonketotic hyperosmolar coma ***
30
Q

Describe the genetic difference between type 1 and type 2 diabetes

A

Type 1

  • 30-70% twin concordance
  • Linkage to MHC class II HLA genes

Type 2

  • 50-90% concordance in twins
  • No HLA linkage
31
Q

Describe the pathogenesis difference between type 1 and type 2 diabetes

A

Type 1

  • Autoimmune destruction of beta cells mediated by T cells
  • ABSOLUTE *** insulin deficiency

Type 2

  • Insulin resistance in skeletal muscle, adipose tissue and liver
  • Beta cell dysfunction and relative insulin deficiency
32
Q

Describe the pathology difference between type 1 and type 2 diabetes

A

Type 1

  • Insulitis early
  • Market atrophy and fibrosis
  • Beta cell depletion

Type 2

  • No insulitis ***
  • Focal atrophy and amyloid deposition ***
  • Mild beta cell depletion
33
Q

What is the most common underlying cause of diabetic complications?

A

KNOW THIS

Non-enzymatic glycation of extracellular matrix
is the MOST common underlying cause
in the pathogenesis of complications in DM

34
Q

Describe pancreatic neuroendocrine tumors (NETs)

A
  • Much less common than adenocarcinomas of the exocrine pancreas
  • Accounts for ony 2% of pancreatic neoplasms
  • When functioning, they produce distinct clinical syndromes related to the peptide hormone they produce
35
Q

What are the three most common and distinctive clinical syndromes associated with functioning pancreatic NETs?

A

1 - Hyperinsulinism (insulinoma)
2 - Hypergastrinemia (Zollinger-Ellison syndrome)
3 - Multiple endocrine neoplsia 1 (MEN 1) syndrome (Wermer syndrome)

He said, “KNOW EVERYTHING about NETs”

36
Q

What is an insulinoma?

A
  • A beta-cell tumor
  • They are the MOST common pancreatic NET
  • May be responsible for the elaboration of sufficient insulin to induce clinically significant hypoglycemia
37
Q

What is the characteristic WHIPPLE TRIAD of insulinomas?

A

1 - attacks of hypoglycemia that occur with blood glucose levels of less than 45
2 - attacks consist principally of CNS manifestations (confusion, stupor, loss of consciousness)
3 - attacks are preceipitated by fasting or exercise and promptly relieved y food (or IV administration of glucose)

KNOW THE TRIAD ***

38
Q

Describe the morphology of insulinomas

A
  • Most often found within the pancreas
  • Can be found anywhere in the pancreas (head, body, tail)
  • Generally benign
  • Most are solitary
  • Usually small (often less than 2 cm)
  • Encapsulated pale nodules
  • Look remarkably like “giant islets”
  • They are carcinomas (malignant tumors) in only 10% of cases
39
Q

How are insulinomas described?

A
  • Small circumscribed homogenous tumors

- Uniform cells found in nests

40
Q

What other cellular structure do we find in insulinomas?

A

Amyloid is often found in insulinomas

Patients with insulinomas, particularly small ones have excellent prognosis

41
Q

What is the second type of pancreatic neuroendocrine tumor (NET) we will talk about (and the only other one we will focus on)?

A

Gastrinomas

Called Zollinger-Ellison syndrome

42
Q

Describe gastrinomas of Zollinger-Ellison syndrome

A
  • Pancreatic gastrinoma is a neuroendocrine tumor that consists of so-called “G cells” that secrete gastrin
  • Patients with Zollinger-Ellison syndrome develop multiple peptic ulcerations in the stomach, duodenum and even jejuum as a result of elevated gastric acid secretion caused by a gastrin-secreting tumor (“gastrinoma”)
43
Q

Describe the ulcers of patients with Zollinger-Ellison syndrome

A
  • Ulcers are present in almost all patients with Zollinger-Ellison syndrome
  • They are identical to the usual peptic ulcerations except that they are often MULTIPLE, found in UNUSUAL LOCATIONS (i.e. jejunum) and may be more difficult to control
44
Q

What population do we commonly see Zollinger-Ellison syndrome in?

A
  • Gastrinomas are most often found in patients between the ages of 30-50, which a slight male predominance
45
Q

Describe the behavior of gastrinomas

A
  • Gastrinomas may have a benign behavior, but many are malignant and capable of local invasion and metastasis to the LYMPH NODES and LIVER (more commonly the liver)
46
Q

Describe the gastrinomas of Zollinger-Ellison syndrome

A
  • Usually a single tumor
  • Hypersecretion of gastric acid and multiple severe gastric and duodenal peptic ulcers are present in 90-95% of patients
  • When intractable peptic ulcers occur in unusual locations such as the jejunum, Zollinger-Ellison syndrome should be considered

** Commonly missed diagnosed **

47
Q

Describe the tendency of gastrinomas to metastasize

A
  • Over half of gastinomas are locally invasive or have already metastasized at the time of diagnosis
  • Most are low-grade, but the only way to tell is whether it has metastasized
48
Q

Describe the tendency of gastrinomas to occur with MEN 1 syndrome

A
  • Approximately 25% of cases arise in conjunction with other endocrine tumors
  • An example is in MEN 1 syndrome - multiple endocrine neoplasm
  • Frequently multifocal

Endocrine Exam 2 (18 decks)

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