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gen path final > Endocrine part 2 > Flashcards

Endocrine part 2 Flashcards

1
Q

the parathyroid glands are mainly composed of ________ cells. what do these cells do?

A
  • Mostly composed of chief cells

- Secrete parathyroid hormone

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2
Q

what does parathyroid hormone control?

A

regulator of blood calcium levels

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3
Q

Besides chief cells, parathyroid glands also contain ______ cells

A

oxyphil

  • they have an unknown function
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4
Q

where are the parathyroid glands located?

A
  • Four small glands

- located on the POSTERIOR surface of the thyroid gland

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5
Q

A decreased level of ________ stimulates the synthesis and release of PTH

A

blood calcium

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6
Q

what are the specific actions of PTH?

A

↑ renal tubular reabsorption of calcium
↑ urinary phosphate excretion
↑ the renal conversion of vitamin D into its active form
↑ osteoclastic activity which releases calcium from the bones

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7
Q

what is the overall function of parathyroid hormone?

A

↑ level of free calcium which inhibits further PTH secretion

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8
Q

________________ is an important cause of hypercalcemia

A

hyperparathyroidism

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9
Q

name the 2 types of hypoparathyroidism, and what causes each:

A
  • Primary
    caused by an autonomous spontaneous overproduction of PTH
  • Secondary
    A secondary phenomenon in pts with chronic renal failure
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10
Q

Primary Hypoparathyroidism is usually the result of what 2 disorders?

A

Usually the result of:

A) parathyroid hyperplasia (multiglandular)

B) an adenoma (solitary)

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11
Q

what groups are most likely to have PRIMARY hyperparathyroidism?

A

1) Adults

2) Women (4X as likely as men)

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12
Q

what are the “Classic clinical features” of PRIMARY Hyperparathyroidism?

A

“Painful bones, stones, abdominal groans, and psychic moans”

  • fractures from osteoporosis
  • kidney stones
  • constipation, ulcers, gallstones
  • depression/lethargy/seizures
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13
Q

T/F: most cases of primary hyperthyroidism are diagnosed after clinical signs appear

A

FALSE

  • clinically silent hyperparathyroidism is detected early
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14
Q

Secondary hyperparathyroidism is usually the result of what?

A

Usually due to renal failure

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15
Q

what is hyperphosphatemia ? how does it lead to the production of PTH?

A

= increased amounts of phosphate in the blood because of decreased excretion

  • that decreases serum calcium
  • decreased serum Ca = increased PTH
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16
Q

Renal failure not only leads to hyperphosphatemia, but also to the failure to synthesize ______

A

vitamin D

This reduces calcium absorption in the intestines

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17
Q

Clinical characteristics of Secondary hyperparathyroidism:

A

Calcium levels are usually near normal

Symptoms dominated by renal disease

Renal osteodystrophy (growth of bone)

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18
Q

why are serum calcium levels usually within the normal range during secondary hyperparathyroidism?

A

Compensatory increase in PTH levels sustains serum Ca

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19
Q

treatments for Hyperparathyroidism :

A

Surgical removal of hyperplastic parathyroid glands

Kidney transplant may be beneficial

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20
Q

T/F: Hypoparathyroidism is more common than Hyperparathyroidism

A

FALSE

hyper = common

hypo = uncommon

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21
Q

causes of hypoparathyroidism:

A

A) Surgically induced, removed during thyroidectomy
B) Congenital absence
C) Autoimmune

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22
Q

what is Di George Syndrome?

A

congenital absence of parathyroid glands

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23
Q

clinical signs of hypothyroidism:

A

1) Hypocalcemia
2) Increased neuromuscular excitability
3) Cardiac arrhythmias
4) Increased intracranial pressure and seizures

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24
Q

The endocrine pancreas is composed of the _____________________

A

islets of Langerhans

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25
Q

what are the 4 major cell types of the islets of langerhans? what is the function of each type

A

Beta cells: produce insulin

Alpha cells: produce glucagon

Delta cells: produce somatostatin

PP cells: produce VIP, a pancreatic polypeptide

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26
Q

Somatostatin suppresses both __________ and _________ release

A

insulin and glucagon

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27
Q

VIP (a peptide produced by the pancreas) exerts several effects on what?

A

the G-I tract

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28
Q

_____________ is a group of metabolic disorders resulting in hyperglycemia (excessive amounts of glucose in the blood)

A

Diabetes Mellitus

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29
Q

Diabetes Mellitus is the leading cause of what other medical conditions?

A

Leading cause of:

  • ESRD (renal failure)
  • blindness
  • lower limb amputation
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30
Q

what are normal blood glucose levels? what levels do diabetics have?

A

Normal = 70-120 mg/dL

Diabetic if either:

1) A random glycemia of ≥ 200mg/dL
2) Fasting glucose levels of ≥ 126mg/dL
3) abnormal glucose tolerance test

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31
Q

what causes type 1 diabetes? what does it result in?

A

Beta cells of the pancreas get destroyed by self-reactive T cells & autoAntiboides

Results in absolute deficiency in insulin production

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32
Q

Clinical features of Type 1 diabetes:

A
  • diagnosed before age 20 in patients who have a normal weight
  • Characterized by decreased blood insulin
  • autoAbs are detectable in the blood of 70-80% of pt’s
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33
Q

name the 4 symptoms of type 1 diabetes:

A

1) Polydipsia (thirsty)
2) Polyuria (peeing)
3) Polyphagia (hungry)
4) Ketoacidosis (acetone breath)

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34
Q

what is the prognosis for type 1 diabetes?

A

guarded

  • because of all the possible complications
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35
Q

T/F: Type 2 diabetes is an autoimmune-related disease

A

FALSE

it is NOT autoimmune

36
Q

type 2 diabetes may be the result of what 2 conditions?

A

1) Insulin resistance (failure of target tissues to respond normally to insulin)
2) Decreased insulin secretion (may be normal in amount, but inadequate for the patient’s size if they are obese)

37
Q

clinical features of type 2 diabetes:

A

1) Onset after age 40 (usually, but not always)
2) Obesity
3) Insulin levels in the blood may be normal or increased
4) Increased susceptibility to infection, periodontal disease

38
Q

the symptoms of Type 2 diabetes are the same symptoms as type 1, but it is rare to have ______________

A

ketoacidosis

mainly found in type 1

39
Q

Type 1 diabetes makes up ____% of all diabetes forms

A

10%

the other 90% is type 2

40
Q

what happens to the pancreas during diabetes mellitus?

A
  • Destruction of Islets
  • Heavy inflammatory infiltrate
  • Amyloid (protein fragments)
41
Q

_____________ is responsible for 80% of the diabetes related deaths

A

Vasculopathy

42
Q

what types of vasculopathy can result from Diabetes mellitus?

A

A) Atherosclerosis
B) Myocardial infarction, stroke
C) Gangrene of lower extremities
D) Microangiopathy (thickening of basement membrane)

43
Q

diabetic nephropathy is the 2nd most common cause of diabetes-related death, and leads to what 2 conditions?

A

leads to:

1) hypertension
2) end stage renal disease (ESRD)

44
Q

characteristics of Diffuse glomerulosclerosis:

A

A) 90% of diabetics within 10 years; not specific to diabetics

B) Microangiopathy around glomerular capillaries and deposition of matrix

C) Proteinuria, total renal failure

45
Q

Characteristics of Nodular glomerulosclerosis:

A

A) 15-30% of persons with long-term diabetes

B) Ball-like deposition of matrix at the periphery of the glomerulus

C) Total renal failure

46
Q

which form of glomerulosclerosis is specific to diabetics?

A

Nodular glomerulosclerosis

47
Q

in which form of glomerulosclerosis would you see protienurea?

A

Diffuse glomerulonephritis

48
Q

__________ due to diabetes is the 4th leading cause of blindness

A

Retinopathy

49
Q

characteristics of diabetic retinopathy:

A
  • Microangiopathy and microaneurysms

- Retinal detachment and vision loss

50
Q

what 2 types of nerves are effected by diabetic neuropathy?

A

1) Can affect the peripheral sensorimotor nerves

2) Autonomic neuropathy

51
Q

what are the clinical manifestations of diabetic autonomic neuropathy?

A
  • causes disturbances in bowel and bladder function

- sexual impotence

52
Q

what types of infections are more likely in patients with diabetes?

A
  • infections of the skin
  • TB, pneumonia
  • deep fungal infections
  • pyelonephritis
53
Q

T/F: most Islet cell tumors arise from the endocrine pancreas

A

FALSE

most are from exocrine pancreas

54
Q

______________ are functional tumors that arise in duodenum, peripancreatic tissues, or pancreas

A

Gastrinomas

55
Q

characteristics of gastrinomas:

A
  • gastric acid hyper secretion
  • cause 90-95% of recalcitrant peptic ulcers
  • cause Zollinger-Ellison Syndrome
56
Q

what is Zollinger-Ellison Syndrome? how is it treated?

A
  • Pancreatic islet cell tumor that causes
    1) hypersecretion of gastric acid
    2) severe peptic ulcers
  • Most are MALIGNANT (60%)
  • treated by surgical resection
57
Q

name the hormones secreted by the adrenal cortex:

A

1) Cortisol/cortisone
2) Aldosterone
3) Estrogen and Progesterone

58
Q

what is secreted by the adrenal medulla?

A

Catecholamines

  • Epinephrine (adrenaline)
  • Norepinephrine
  • Dopamine
59
Q

T/F: the outer portion of the adrenal gland produces hormones, while the inner portion produces catecholamines

A

true

60
Q

what are the 2 types of hyperadrenalism?

A

1) Hypercortisolism (Cushing Syndrome)

2) Hyperaldosteronism

61
Q

Name the causes of Cushing’s Syndrome:

AKA Hypercortisolism

A

A) Excess administration of exogenous glucocorticoids

B) Primary adrenal hyperplasia or neoplasm

C) Primary pituitary source

D) Ectopic ACTH secretion by neoplasm

62
Q

what is Cushing’s DISEASE?

A
  • hypercortisolism due to primary pituitary source

- ACTH oversecretion

63
Q

what site is a common ECTOPIC source of ACTH secretion? (that causes cushing’s)

A

the lungs

called “paraneoplastic cushing’s syndrome”

64
Q

____________ cushing’s syndrome is caused by ingestion of exogenous glucocorticoids

A

Iatrogenic cushing’s syndrome

65
Q

Short term effects of Cushing’s syndrome:

A

A) weight gain and hypertenstion

B) “Moon face” (accumulation of fat in the face)

C) “Buffalo hump” (accumulation of fat in the posterior neck & back)

66
Q

what are the 2 “main” features of long-term Cushing’s syndrome?

A

Osteoporosis

mood swings

67
Q

what is the result of Hyperaldosteronism ?

what effect does excess aldosterone have

A

Sodium retention, potassium excretion

Hypertension and hypokalemia

68
Q

characteristics of Primary Hyperaldosteronism:

A

Very rare

Hyperplasia, neoplasm, idiopathic

**Decreased levels of plasma renin

69
Q

characteristics of secondary Hyperaldosteronism:

A

Aldosterone release in response to activation of renin-angiotensin system

**Increased levels of plasma renin

70
Q

what causes secondary hypoadrenalism?

A

Decreased stimulation of adrenals from deficiency of ACTH

71
Q

secondary hypoadrenalism does not appear until ____% of adrenal gland has been destroyed

A

90%

72
Q

what causes Acute Adrenocortical Insufficiency?

A
  • occurs in patients that abruptly stop taking exogenous steroids
  • rapid withdrawal of steroids or failure to increase steroids in response to an acute stress can precipitate an adrenal crisis

Can also be caused by adrenal hemorrhage or stress

73
Q

effects of Acute Adrenocortical Insufficiency:

A
  • Vomiting, abdominal pain, hypotension, coma, death
74
Q

Acute Adrenocortical Insufficiency can also be triggered by stress in patients with ______________

A

Addinson’s disease

75
Q

what is Addison’s disease?

A
  • Primary Chronic Adrenocortical Insufficiency
  • Progressive destruction of adrenal cortex
  • Destruction of cortex prevents response to ACTH
76
Q

clinical characteristics of Addison’s Disease:

A

A) Hyper-pigmentation (due to increased serum ATCH)
B) Progressive weakness
C) GI disturbances
D) craving for salt

77
Q

causes of Addison’s disease:

A

1) Autoimmune destruction of steroid-producing cells
* Most common, 60-70% of cases**

2) TB
3) AIDS
4) Metastatic disease

78
Q

what is the definition of Secondary Adrenocortical Insufficiency?

A

Any disorder of hypothalamus of pituitary that reduces output of ACTH

79
Q

what key clinical sign is MISSING in patients with secondary adrenocortical insufficiency?

(its in primary, but not secondary)

A

no skin/mucosa pigmentation

primary will have ELEVATED ACTH, secondary will have lowered production

80
Q

characteristics of Pheochromocytomas:

A
  • neoplasm of chromaffin cells (adrenal glands)
    - these cells make epinephrine
  • F > M, 30-60 yrs
  • ** Hypertension
  • surgically correctable
81
Q

what percent of Pheochromocytomas are malignant? bilateral? extra-adrenal? familial?

A

each category has a 10% prevalence

  • its why Pheochromocytomas are called the “10% tumor”
82
Q

what are the 3 types of Multiple Endocrine Neoplasia (MEN) Syndromes

A

Types I, 2A, and 2B

83
Q

Multiple Endocrine Neoplasias appear in what organs?

A 
o	Medullary Thyroid Carcinoma
o	Pheochromocytoma (chromaffin cells)
o	Parathyroid 
o	Pituitary
o	Pancreas
84
Q

what proto-onconogene is mutated in patients with MEN?

mult endocrine neoplasias

A

RET proto-onconogene

85
Q

Mult endocrine neoplasia type 2B notable for its ________ manifestations

A

orofacial

86
Q

characteristics of type 2B MEN:

A
  • Mucosal neuromas (tongue, labial commisure)
  • Large, blubbery lips
  • Marfanoid body habitus

gen path final (8 decks)

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