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ALU 201 > Chapter 9 > Flashcards

Chapter 9 Flashcards

1
Q

Define hormones

A

Peptides that are secreted into the bloodstream and act on target tissues which have receptors.

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2
Q

What is the difference between the following hormone systems:

  1. endocrine pathway
  2. autocrine pathway
  3. paracrine pathway
A
  1. act on site distant from gland
  2. acts locally on adjacent tissue
  3. act reciprocally on the gland from which it originated
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3
Q

How is hormone secretion controlled?

A

Feedback loop`s

negative vs positive

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4
Q

what does the pituritary gland control? What controls the pituritary gland?

A

regulates: adrenal gland, thyroid gland, ovary, testes, affects liner growth, fuel metabolism, water balance, pregnancy and lactation.

Its controlled by the neuronal and chemical input from the hypothalamus.

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5
Q

What is prolactinoma?

A

benign tumor of lactotroph cells.

there is a clonal proliferation of lactotroph and causes unregulated secretion of prolactin.

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6
Q

what is the clinical presentation of prolactinoma?

A

differs from M to F and size of tumor.
F with micro = menstrual irregularities and galactorrhea
M with macro= loss of libido and impotency

large tumors cause headaches and visual disturbances if compression on the optic chiasm.

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7
Q

whats the difference between microadenoma and macroadenoma?

A 
micro= <10mm 
macro= >10mm  * mortality increases for those with this if the hypopituitarism develops
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8
Q

how is prolactinoma treated?

A 
small = restoring normal mentrual cyst and potency in males
large= removed surgically or tx'ed with external beam radiation.  risk ' destruction of remaining gland and hypopituitarism
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9
Q

Define hypopituitarism

A

developed after surgery of pituitary tumors or any destructive process of the pituitary.

pt require replacement with cortisol, thyroid hormone, sex hormones. GH therapy may also be required

mortality risk ^^

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10
Q

Define Diabetes Insipidus.

A

the result of lack of antidiruetic hormone (vasopressin) that is produced in the hypothalamus and stored/released by posterior pituitary.

controls water absorption- if missing free water is not absorbed causing hypernatremia.

hormone can be replaced by using intranasal, intravenous or oral desomopressin (DDAVP) which restores water balance.

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11
Q

Define Acromegaly

A

disorder caused by a benign tumour of somatotroph cells that produce GH. The secretion is then unregulated and over produced.
sxs: enlarged feet, hands, soft tissue swelling, CTS, HTN, LV enlargement, cadiomyopathy, polyps, sleep apnea, and glucose intolerance.

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12
Q

What does GH do?

A

stimulates production of insuling-like growth factor-I. ( IGF-I )

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13
Q

What regulates the production and release of thyroxine (T4) and tri-iodothyronine (t3) from the thyroid gland?

A

Hypothalamic-pituitary axis

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14
Q

What does T4 and T3 do?

How is it transported in the system?

A

they inhibit TRH and TSH release by feedback system trought the hypothalamus and pituitary.

T4 secreted from thryoid, and converted into T3 in paripheral tissues. Theyre carried through the system on thyroid binding globulin, albumin and pre-albumin.

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15
Q

There are specific T4 and T3 receptors that result in the activation of different cellular processes. What are they?

A
  1. increased O2 consumption
  2. stimulation of protein synthesis
  3. enhanced lipolysis.
  4. enhanced response to epinephrine and noreepine
  5. increased HR and contractility
  6. increased growth and development
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16
Q

How is a thyroid disorder diagnosed?

A

usually through BW to detect abN hormone levels. ie: Total T4, thyroid binding globulin, free thyorixine index, and TSH.

Can also look at thyroid directly and funtion with u/s, CT, MRI, radioiodine uptake scan, and technetium scans.

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17
Q

What is hyperthyroidism?

A

a constellation of clinical sxs resulting from excess T4 and/or T3.

sxs: reflect heighened sympathetic nervoius system and metabolic activity. (think high on uppers)

if untx’d can result in thyroid storm.

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18
Q

What is thryoid storm?

A

life-threatening condition of thyroid excess that results in end organ damage.
body stays in “combat crissis”

sxs: hyperthermia, cardiac arrhythmia, malignant HTN, coma, Seizures. hepatic failure

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19
Q

What is a common cause of hyperthyroidism?

A

graves disease.
its caused by autoimmune stimulation to the thyroid gland.
its tx’ed with Rx, ablative doses of radioiodine, or occasionally surgery.

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20
Q

Define hypothyroidism

A

insufficient T4/T3 with sxs and signs of decreased sympathetic nervous system and metabolic activity.

gradual prognosis

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21
Q

What happens when hyperthyroidism goes untreated?

A

risk of myxedema coma. A life threatening condition, which involves a multi-organ collapse. Its rare.

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22
Q

What is a common cause for hypothyroidism

A

Hashimotos thyroiditis, an autoimmune attack on the thyroid gland. A destructive process that leads to impaired synthesis and release of thyroid hormone.

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23
Q

When does a thyroid nodule cause a concern ?

A

single solid nodules grater or equal to 1 cm. Thyroid cancer is a “cold” nodule on radioiodine uptake scan. There should have a FNA to determine a course of action.

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24
Q

Define the physiology of the adrenal gland

A

located in space overlying kindey
composed of distinct cell types. Outter portion is divided into 3 zones.
1. glomerulosa that produces aldosterone
2. fasiculata produces cortisol
3. reticularis that produces androgens

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25
Q

What part of the adrenal gland produces epinephrine and noreepinephrine
?

A

the center of the adrenal gland. Its called the medulla.

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26
Q

What does ACTH from the pituitary gland do?

A

affects the production of cortisol and androgens. also partially controls release or epi/norepinephrine.

27
Q

what controls the secretion of aldoesterone?

A

renin, potassium and intravascular volume status.

28
Q

What is primary hyperaldosteronism?

A

overproduction of aldosterone by the flomerulosa cells of the adrenal gland leads to the development of HTN.
Associated with low levels of K+ excretion.
sxs: muscle weakness, fatigue, thirst,

29
Q

What are the two most common etiologies of primary hyperaldosteronism

A
  1. aldosterone-producing adenoma

2) bilateral adrenal hyperplasia.

30
Q

How is primary hyperaldosteronism treated?

A
  1. aldosterone-producing adenoma: surfical removal
    2) bilateral adrenal hyperplasia: use of anithypertensive Rx that blocks effect of aldosterone on the kidneys (spironolactone)

> > Tx the HTN

31
Q

What is hypercortisolism (Crushing Syndome is the most common cause (60%), also caused by primary adrenal tumor secreting excessive cortisol or ectopic production of ACTH from a small cell carcinoma of the lungs)

A

overproduction of cortisol which causes hypersecretion of ACTH from a pituitary microadenoma.
sxs: truncal obesity, moon facies, buffalo hump, etc.

tx: tx cause, either by surgery, bilateral adrenalectomy, Rx or external beam radiation.

32
Q

What can cause adrenal insufficiency?

A
  1. primary destruction of the adrenal glands

2. secondary insufficiency (lack of ACTH or its suppressing hormone)

33
Q

In the example of Addison’s disease, how can the adrenal glands be destroyed? (4)

A
  1. autoimmune attack
  2. infections with HIV, tuburculosis or histoplasmosis
  3. metastatic spread of cancer
  4. hemorrhage
34
Q

what causes secondary adrenal insufficiency?

A

d/t exogenous use of supraphysoilogic amount of steroids that are given for other dieases, this supresses the ACTH production.

35
Q

What are the sxs of adrenal insufficiency?

A

weakness, fatigue, nausea, vomiting, abdo pain, joint pain, muscle tenderness, dizziness. Can be life threatning.

36
Q

What is pheochromocytoma

A

A tumor of chromaffin-containing cells that produce excess epinephrine and norepinephrine.

sxs: headache, perspiration and palpitations, HTN, arrhythmias high output congestive heart failure.
tx: surgery to remove tumor. VERY DIfficult. if malignant prognosis is bad, if not, its okay.

37
Q

Whats the difference between the terms pheochromocytoma and paraganglioma

A 
pheochromocytoma = tumors specifically found in the adrenal medulla
paragranglioma= tumors located in chromaffin tissue outside the adrenal.
38
Q

Define the physiology of the parathyroids

A

4 pea-sized glands located near thyroid, that produce PTH, which regulates serum calcium concentration.
acts mostly on kidney, bone and intestine tissues.

39
Q

What is hyperparathyroidism?

A

excessive production of PTH -> hypercalcemia.

usually caused by single parathyroid adenoma (85%), 4-gland hyperplasia (15%).

40
Q

What is hypercalcemia?

A

causes polyuria, thurst, addo pain, stones mental confusuion, coma. Longstanding dx leads to osteoporosis.

tx: sxs. People with severe osteoporosis, stones, renal damace, or ^ Ca+ require surgery to remove adenoma or hyperplastic glands.

41
Q

how is parathyroid cacinoma treated?

A

its incurable, even after surgery.

42
Q

What causes Hypercalcemia of malignancy?

how is it tx’ed?

A
  1. elaboration of parathyroid hormone-related peptide by the tumor
  2. metastasis to bone, causing bone resorption and release of Ca+ from the bone
  3. both 1 and 2.

tx to reduce Ca+ levels, with saline hydration, furosemide calciuresis and done antriresorptive therapy.

Very poor prognosis

43
Q

Hyperparathyroidism can be seen with the familial syndromes of multiple endocrine neoplasia (MEN). There are 3 kinds of syndromes with different combinations of disorders. Name them.

A
  1. MEN 1
    a) primary hyperparathyroidism
    b) pituitary adenomas
    c) pancreatic tumors
  2. MEN 2A
    a) medullary carcinoma of the thyroid
    b) pheochromocytoma
    c) primary hyperparathyroidism
  3. MEN 2B
    a) medullary carcinoma of thyroid
    b) pheochromocytoma
    c) marfanoid body habitus, intestinal ganglioneuromas
44
Q

What causes MEN syndromes?

A

inherited DNA mutations.

dx can now be made with blood test in those with Fx.

45
Q

Which hormones regulate normal glucose levels?

A
  1. insulin *(key)
  2. glucagon * (key)
  3. somatostatin
  4. cortisol
  5. epinephrine
  6. growth hormone
46
Q

How does insulin (beta cell release) and glucagon (alpha cell release) act on glucose?

A

insulin promotes glucose utilization by increasing tissue uptake of glucose and stimulating glycogen synthesis. activated by food for food use and utilization
Glucagon used to counter-balance insulin- fasting use. by stimulating the formation of glucose from stored glycogen, free fatty acids, or amino acids.

47
Q

What is Sematostatin?

A

secreted from delta cells in the pancreatic islets and inhibits both insulin and glucagon. This prevents rapid exhaustion of glucose when meal is eaten

48
Q

What is Diabetes Mellitus ?

A

disorder of glucose metabilism.

caused by either absolute or relative lack of insulin (nt working).

49
Q

What the 5 methods of Diabetes Diagnosis?

A
  1. fasting blood glucose >126 on 2+ occasions
  2. glucose >200 any time of day
  3. a glucose >200 or equal too at any time during oral glucose tolorence test
  4. A1C >6.5%
  5. evidence of acute diabetic ketoacidosis or hyperosmolar coma with extreme hyperglycemia.
50
Q

How is IFG and IGT defined?

A

IFG: glucose >100 but less or equal to 125
IGT: blood glucose >140 but <200 at any time during glucose tolerance test.

51
Q

What are the 4 main kinds of DM?

A
  1. type 1
  2. type 2
  3. other
  4. gestational
52
Q

Define Type 1 DM

A

caused by autoimmune destruction of the pancreatic beta cells. There is absolute insuling deficiency, and insuling injections are required for survivial. by pump or needle.

  • common in <21 yo.
  • slight genetic co-factor
  • daily blood sugar monitoring required.
53
Q

Define T2 DM

A

relative lack of insulin or state or insulin resistance.

  • usually caused by obesity
  • intime pancreatic beta cells may exhaust and insulin may be required. Tx is otherwise diet, weight loss and Rx.
  • higher genetic predisposition
54
Q

Define “other” causes of DM

A

possible causes:

  1. rare disorder of insulin receptors
  2. disorder of insulin binding
  3. diabetes mellitus
  4. pancreatis destruction
  5. crushing syndrome
  6. MODY
55
Q

Define MODY

A

autosomal dominant form of maturity onset diabetes of youth. Involves mutation of the sensing of glucose load by beta cells.

  1. MODY 1- defect in hepatic nuclear factor 4
  2. MODY 2- a defect in glucokinase enzyme
  3. MODY 3- defect in hepatic nuclear factor 1.

sxs: defect in secretion of insulin, tirggered by episode of DKA .
tx: DKA control and tx’ with insulin until beta cells recover. then can revert to diet/Rx control.

56
Q

Define Gestiational DM

A

diabetes that occurs during pregancy.

dx: blood test during pregnancy check-up, if glucose >140, futher testing is completed. 3 measurements taken, if 2 are over, dx is confirmed.
tx: stabalize glucose levels. Insulin is only option.

Increases risk of T2DM in mother.

57
Q

What are the 3 typical acute complications of DM?

A
  1. diabetic detoacidosis
  2. Diabetic hyperosmolar coma
  3. acute hyperglycemia

** alll have ^ mortality risk.

58
Q

What are the chronic complications of DM?

A

depends on the degree of glucose control and duration of disease. Divided into 2 kinds

  1. complications related to microvascular disease- retinopathy, nephropathy and neuropathy
  2. complications related to macrovascular disease- hypertrophic arterial vessels.
59
Q

How is DM monitored?

A
  1. following A1C levels [3 mo. history marker]
  2. Fructosamine levels- correlated with A1C but more prone to false readings [10-20 days history marker]
  3. Glycomark [new]- measured 1,5 anhydroglucitol and is useful for evaluating postprandial glucose levels.
60
Q

Do retinopathy and neuropathy disorders develop as an onset or in stages?

A

in stages. Good glucose control can prevent the development and progression.

Most Diabetes will develop retinopathy, only some will develop nephropathy- but this is worse.

61
Q

Is Neuropathy a common complication?

A

yes.
peripheral: involves destruction of both small (senses) and large nerve fibers (movement).

diabetics with cardiac autonomic neuropathy have very high mortality.

62
Q

Define hypoglycemia

A

low blood glucose. Defined by

  1. sxs of low blood glucose
  2. sxs must correspond to documented low blood glucose
  3. sxs must resolve with the administration of glucose.

sxs: affect activation of sympathetic nervous system and lack of glucose to the brain. Tachycardia, sweating, palpitations, confusion, neurological deficits, coma.

63
Q

There are two kinds of hypolycemias

A
  1. reactive - fall in blood glucose occurs several hours after eating.
  2. fasting: occurs in absence of food and is usually indicative of a more serious disorder.

Difference in dx is broad but includes: pancreatic insulin-producing tumor, liver failure, undx Addisons disease, undx’ed hypopituitarism, ETOH intoxication, renal failure, sepsis, neoplasms which secrete insulin-like growth factor 2.

64
Q

How is metabolic syndrome characterized?

A

presence of impaired glucose handling, proatherosclerotic lipid profile, HTN and abdominal obesity.
Requires 3 or more of the following disorders:
1. waist circumference ^ / ^ BMI
2. ^ TRIGS
3. L HDL
4. ^ BP
5. ^ fasting glucose / ^ microalbuminuria

> > Dx = ^ risk of morbidity and mortality

Tx: with diet, exercise, weight loss, HTN control, lipid control and glucose control. Rx may be used,

ALU 201 (16 decks)

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