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Pathology > Endocrine Part II > Flashcards

Endocrine Part II Flashcards

1
Q

What is the Incretin effct?

A

oral intake of food leads to secretion of multiple hormones that play a role in glucose homeostasis & satiety

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2
Q

what are the hormones released during Incretin effect and where are they secreted from?

A

Glucose-dependent insulinotropic polypeptide - K cells in the proximal small intestine

Glucagon-like peptide-1 = L cells in the distal ileum and colon

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3
Q

What mediates glucose u[tale by GLUT4 to the plasma membrane?

A

AKT - principle effector of the PI3K pathway
CBL - direct phosphorylation target of the Insulinr eceptor

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4
Q

What are the chances of u developing DM with first-degree relatives with DM?

A

5 to 10 fold higher risk

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5
Q

What are adipokines that decrease blood glucose by INC insulin sensitivity in peripheral tissues?

A

Leptin & Adiponectin

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6
Q

What adipokine is reduced in obesity thus contributing to insulin resistance?

A

Adiponectin

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7
Q

What can happen when there is an excessive FFA?

A

impedes insulin signaling directly within peripheral tissues or indirectly through the release of pro-inflammatory cytokines

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8
Q

what happens if there is excess FFAs within macrophages and B cells?

A

Activates Inflammasome –> secretion of the cytokine IL-1B

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9
Q

What is the function of IL-1B and IL-1?

A

IL-1B = mediates secretion additional pro-inflammatory cytokines

IL-1 and other cytokines = released into the circulation and act on the major sites of Insulin action to promote Insulin resistance

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10
Q

What are diff mechanisms that promote B cell dysfunction?

A
  1. Excess FFA compromising B cell function and Insulin release
  2. Impact of chronic hyperglycemia
  3. Abnormal “incretin effect” which leads to reduced secretion of GIP & GLP-1
  4. Amyloid deposits in the islets
  5. Genetics
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11
Q

what are the monogenic forms of DM?

A

Genetic defects in B cell function
Genetic defects in Insulin action

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12
Q

What are the genetic defects in Insulin action?

A

Type A insulin resistance = Acanthosis nigricans
Lipoatrophic DM = hyperglycemia w/ loss of adipose tissue

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13
Q

What are the 4 harmful effects of persistent hyperglycemia?

A
  1. Formation of advanced glycosylation end product
  2. Activation of protein kinase C
  3. Oxidative stress and disturbances in the polyol pathway
  4. Hexosamine pathway and formation of fructose-6-phosphate => exacerbates end organ damage
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14
Q

What is the histological presentation in DM type I & II?

A

Type I = INC in # of Islet cells, leukocytic infiltrates in the islets
Type II = Subtle reduction in islet cell mass, amyloid deposit in the islets –> expression of B cell exhaustion

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15
Q

What happens in diabetic macrovascular disease?

A

Endothelial dysfunction
- Accelerated atherosclerosis = Coronary artery (MI)
- Hyaline atherosclerosis: arterioles in Small BVs in the kidney

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16
Q

What histologic presentation is seen in diabetic microangiopathy disease?

A

Diffuse thickening of the BM –> capillaries of skin, skeletal muscle, retina, glomeruli, renal medulla

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17
Q

What are the 3 lesions formed from diabetic nephropathy?

A
  1. Glomerular lesion
  2. Renal vascular lesion
  3. Pyelonephritis
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18
Q

What is Kimmelstiel-Wilson lesion?

A

nodular glomerulosclerosis

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19
Q

What happens if renal vascular lesion & pyelonephritis progress?

A

Renal vascular lesion = arteriosclerosis
Pyelonephritis= necrotizing papilitis

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20
Q

What condition in the kidneys can occur if there is long standing DM? WHat does it look like (gross)?

A

Nephrosclerosis
- Diffuse granular transformation of the surface
- marked thinning of the cortical tissue
- irregular depression
- incidental cortical cyst

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21
Q

What are the different diabetic ocular complications?

A

Cataract –> disturbance of polyol pathway
Glaucoma
Retinal vasculopathy of DM

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22
Q

What are the complications of diabetic peripheral neuropathy?

A

diabetic foot
ulceration
gangrene –> ischemia –> infection –> necrotic –> amputation

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23
Q

What are the clinical manifestation of chronic disease?

A

Macrovascular complication –> MI, renal vascular insufficiency, CVA
Visual impairment –> total blindness
Neuropathy –> distal symmetrical neuropathy
Autonomic neuropathy –> neurogenic bladder
INC susceptibility to infection

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24
Q

What are the different pancreatic endocrine tumors?

A

Hyperinsulinism (Insulinomas)
Zollinger-Ellison syndrome (Gastrinomas)

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25
Q

What are the presentation of Insulinomas?

A

Solitary tumors w/ amyloid deposits –> Focal or diffuse hyperplasia of the Islets

Hypoglycemia

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26
Q

What is the presentation of Zollinger-Ellison syndrome?

A

Gastrin-producing tumors –> gastric acid hypersecretion & peptic ulceration

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27
Q

What are other rare pancreatic neuroendocrine tumors?

A

a-cell tumors (Glucagonomas) –> produce Glucagon
Delta-cell tumors (Somatostatinomas) –> produces Somatostatin
VIPomas –> watery diarrhea, hypokalemia, achlorhydria/WDH syndrome
Pancreatic carcinoids -> produces Serotonin

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28
Q

what are the clinical manifesations of Cushing syndrome?

A

Truncal obesity, moon facies, and accumulation of fat in the posterior neck & back (buffalo hump)

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29
Q

What are the lab tests done to diagnose Cushing syndrome?

A

Increased 24-h urine free-cortisol concentration
Loss of normal diurnal pattern of cortisol secretion

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30
Q

What is a cell pathognomonic to Cushing’s dynrome?

A

Pituitary-Crooke’s hyaline change

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31
Q

In what type of CUshing syndrome can we see diffuse hyperplasia?

A

ACTH-dependent Cushing syndrome

32
Q

What type of hyperplasia are seen in the adrenal glands?

A

Macronodular hyperplasia - lipid-poor & lipid-rich cells
Micronodular hyperplasia - w/ atrophic intervening areas

33
Q

What can cause Cushing syndrome to be malignant or benign?

A

Primary adrenococortical neoplasms

34
Q

WHat are the histological features of an adrenal cortical adenoma?

A

Neoplatic cells are vacuolated bcos of the presence of intracytoplasmic lipids

There is mild nuclear pleomorphism

Mitotic activity & necrosis are not seen

35
Q

What are the 2 kinds of hyperaldosteronism?

A

Primary & Secondary hyperalodsteronism

36
Q

What is the cause of primary hyperalosteronism?

A

Autonomous overproduction of aldosterone with resultant suppression of the RAAS & DEC plasma renin activity

37
Q

What causes secondary hyperaldosteronism?

A

Aldosterone release occurs due to activation of RAAS —> INC levels of plasma renin —> DEC renal perfusion, Arterial hypovolemia & edema, Pregnancy

38
Q

What is the most common manifestation of primary hyperaldosteronism?

A

BP Elevation

39
Q

What is the most common underlying cause of primary hyperaosteronism?

A

Bilateral idiopathic hyperaldosteronism w/ bilateral nodular hyperplasia

40
Q

What condition cayses Adrenocortical neoplasm?

A

Conn syndrome
Aka solitary aldosterone-secreting adenoma

41
Q

What is an uncommon cause of primary familial hyperalodsoteronism?

A

Glucocorticoid-remediable hyperalodsteronism

42
Q

What is the gross morphology of Aldosterone-producing adenomas?

A

Solitary small, well-circumscribed lesions, mroe often found on the L than on the R

Buried within the gland, is not visibly enlarged

43
Q

What are the special cells seen in Aldosterone-producing adenomas?

A

Lipid-laden cortical cells

44
Q

WHat is a characteristic feature of aldosterone-producing adenomoas?

A

Spironolactone bodies

45
Q

What is the most important clinical consequence of hyperaldosteronism?

A

Hypertension

46
Q

What are the long-term effects of hyperaldosteronism-induced HTN?

A

CV compreomise, stroke, MI

47
Q

What confirms diagnosis of primary hyperaldosteronism?

A

Elevated ratios of plasma aldosterone concentration to plasma renin activity

48
Q

What are different adrenogenital syndrome?

A

C-21 hydroxylase deficiency
21-Hydroxylae deficiency - impaired synthesis of both cortisol & aldosterone

49
Q

What are the cause sof C21 hydroxylase deficiency?

A

Adrenocortical neoplasms
Congenital adrenal hyperplasia

50
Q

What causes congenital adrenal hyperplasia? What is its effect?

A

Autusomal recessive inherited metab errors

Effect: INC production of androgens (virilization), INC secretion of ACTH

51
Q

What is the msot common cause of congenital adrenal hyperplasia & what are its 3 primary features?

A

21 hydroxylase deficiency

  1. Salt losing adrenogenitalism - salt-wasting, hyponatremia, and hyperkalemia (acidosis, HTN, CV collapse, death)
  2. Simple virilizing adrenogenitalism syndrome w/o salt-wasting - ambigous genitalia
  3. Nonclassic or late onset adrenal virilism - more common & partial def of 21-hydroxylase function
52
Q

What are the 3 conditions caused by adrenocortical hypofunction?

A

Primary & Secondary adrenal insufficiency
Addison’s disease (Primary chronic adrenocortical insufficiency)

53
Q

What conditions cause primary adrenal insufficiency?

A
  • rapid withdrawal of steroids
  • massive adrenal hemorrhae (Waterhouse-Friederichson syndrome)
  • loss of cortical cells
  • metab failure in hormone production
54
Q

What are cause sof secondary adrenal insufficiency?

A

Hypothalami pituitary disease = neoplasm, inflammation

Hypothalamic pitutiary suppression = long-term steroid administration, steroid-producing neoplasms

55
Q

What are diff conditions that can cause Addison’s disease?

A

Autoimmune adrenalitis
TB, AIDS infections
Metastastic tumors
Genetic causes: CAH, Adrenoleukodystrophy

56
Q

What are conditionc of Primary Chronic Adrenocortical insufficiency/Addison’s dis?

A

Autoimmune polyendocrine syndrome type 1
Autoimmune polyendocrine syndrome type 2

57
Q

In 90% of Addison’s dis, what is the secondary condtion?

A

Tuberculous adrenalitis

58
Q

What causes skin pigmentation in Addison’s dis?

A

Elevated levels of Pro-opiomelanocortin

59
Q

What are the 3 grps of autonomic NS found in extra-adrenal paraganglia?

A

Branchiomeric
Intravagal
Aortico-sympathetic

60
Q

What are neoplasms derived from chromaffin cells?

A

Pheochromocytoma

61
Q

What are the clinical manifestations of Pheochromocytoma?

A

Extra-adrenal -> Paragangliomas
Sporadic
Bilateral Sporadic adrenal pheochromocytoma
Malignant adrenal pheochromocytoma

62
Q

What are Paragangliomas?

A

Pheochromocytomas that develop in extra-adrenal parganglia

63
Q

What is the gross morphology of Pheochromocytoma?

A

Small, circumscribed lesions condined to the adrenal medulla, to large hemorrhagic mass

Well-demarcated large tumors

64
Q

WHat is the histologic morphology of Pheochromocytoma?

A

CLusters of polygonal to SPINDLE-shaped chromaffin cells or chief cells surrounded by supporting sutentanicular rash

“Salt & Pepper” chromatin

65
Q

What cells in Pheochromocytoma are stained with antibodies against S-100?

A

Peripheral sustentacular cells

66
Q

What is the definitive dx of malignancy of Pheochromocytoma?

A

Excusively on the presence of metastasis

67
Q

What are endocine tumors arising in the contect of MEN syndromes? Wjat are the distinct features of this condition?

A

Multiple endocrine neoplasms

Distinct features:
- younger age
- arise in multiple endocrine organ syndronously/metachronously
- multifocal in one organ
- usually prceded by an asymptomatic stage of hyperplasia

68
Q

What are the 3 multiple endocrione neoplasms?

A

MEN 1
MEN 2A
MEN 2B

69
Q

WHat condition is aka Wemer’s syndrome & caused by germline mutations in the MEN1 tumor suppressor gene?

A

MEN 1

70
Q

What does MEN1 do?

A

Encodes a protein called Menin

71
Q

What is the purpose of Menin?

A

It blocks tracriptional activation by JunD when menin partners with JunD

72
Q

What are the abnormalities of MEN1?

A

3Ps

PTG
Pancreas,
Pitutiary gland

73
Q

WHat is the most common manifestation of MEN-1?

A

Primary hyperparathyroidism

74
Q

What is the most commn site of gastrinomas in indiviudal with MEN-1?

A

Duodneum

75
Q

What condition is aka Sipple syndrome tha thas Pheochromcytoma, Medullar carcinoma of the thyroid
Caused by germinal mutation in the RET proto-oncogene on chromosome 10q11.2?

A

Men-2A

76
Q

What is a common presentation in MEN-2A?

A

Medullary carcinoma asosci w. foci of C-cell hyperplasia

77
Q

What is the difference betw MEN-2A & MEN-2B?

A

Hyperparathyroidism is not present in MEN-2B

Pathology (8 decks)

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