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ENDOREPRO MODULE > General Concepts Endo Repro > Flashcards

General Concepts Endo Repro Flashcards

0
Q

What do Alpha cells in the pancreatic islet secrete?

A

Glucagon

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1
Q

What do Beta Cells in the pancreatic islet secrete?

A

Insulin

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2
Q

What do Delta Cells in the pancreatic islet secrete?

A

Somatostatin (SRIF) secreting

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3
Q

What is polydypsia?

A

Excessive or abnormal thirst

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4
Q

What is polyuria?

A

Excessive passage of urine.

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5
Q

What is polyphagia?

A

Excessive eating; gluttony.

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6
Q

What are some acute manifestations of Diabetes Mellitus I?

A 
Polydypsia
Polyuria
Polyphagia
Weight Loss
DKA
Unopposed Secretion of GH and EPI (exacerbating hyperglycemia)
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7
Q

When a patient is insulin deficient (and has excess glucagon) what three pathophysiological phenomenons take place?

A

Decreased glucose uptake
Increased protein catabolism
Increased lipolysis

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8
Q

Decreased glucose uptake in a patient who is insulin deficient will lead to what?

A

Hyperglycemia, glycosuria, osmotic diuresis, electrolyte depletion

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9
Q

What is glycosuria?

A

Presence of glucose in the urine

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10
Q

What is osmotic diuresis?

A

Diuresis resulting from the presence of certain non-absorbable substances in tubules of the kidney such as mannitol, urea, or glucose.

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11
Q

What is diuresis?

A

Increased excretion of urine.

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12
Q

Increased lipolysis in a patient who is insulin deficient will lead to what pathophysiological consequences?

A

Increased plasma FFAs, ketogenesis, ketonuria, ketonemia… ultimately leading to dehydration and acidosis -> coma and death.

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13
Q

What is ketogenesis?

A

Production of ketone bodies

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14
Q

What are ketone bodies?

A

They are normal metabolic products of lipid within the liver (besides acetone which may spontaneously arise from acetoacetic acid) and are oxidized by muscles. Excessive production leads to urinary secretion of these bodies, as in diabetes mellitus.
Substances are acetone, acetoacetic acid, and B-hydroxybutyric acid.

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15
Q

What are three major lab tests you want to consider in terms of diagnosing Diabetes mellitus?

A

Fasting serum glucose
Glucose Tolerance Test
HbA1c (measures long term diabetic control

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16
Q

What is the glucose tolerance test? How is it performed?

A

A test for evaluating the body’s capability to metabolize glucose and based upon the ability of the liver to absorb and store excess glucose as glycogen.
Most common is oral GTT. Sample of blood taken, patient will then be asked to drink a liquid containing a certain amount of glucose (75 grams). Blood will be taken every 30-60 min after drinking solution. Can take up to 3 hrs.

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17
Q

What are characteristics of Diabetes insipidus (DI)

A

Intense thirst
Polyuria
Inability to concentrate urine (due to lack of ADH)

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18
Q

What is a major sign of Diabetes insipidus (DI)

A

Inappropriately dilute urine

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19
Q

What is vasopressin’s function?

A

Concentrate urine

Conserve water

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20
Q

What are the two types of Diabetes Insipidus?

A

Central

Nephrogenic

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21
Q

What is the cause of central DI?

A

Absent or insufficient release of ADH from the posterior pituitary

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22
Q

What are some causes of central DI?

A

Pituitary tumor
trauma
surgery
histiocytosis X

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23
Q

Is ADH secretion normal or abnormal in nephrogenic DI?

A

ADH secretion is normal but the kidneys are unresponsive (renal resistance to ADH)

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24
Q

What are some causes of nephrogenic DI?

A

hereditary or secondary to hypercalcemia, lithium, demeclocycline [ADH antagonist]

25
Q

What is considered the organification step in the synthesis of thyroid hormones?

A

When I2 is attached to tyrosine residues on the primary protein of the follicular luman (thyroglobulin), forming MIT and DIT. It is a TSH mediated step.
Inhibited by PTU and methimazole (both thionamides)

26
Q

Alpha cells of the pancreas secrete what hormone?

A

Glucagon; stimulates hepatic glycogenolysis and gluconeogenesis to increase plasma glucose

27
Q

What is the primary defect in Type 1 Diabetes Mellitus?

A

Deficiency of insulin, typically caused by autoimmune and antibody destruction of the pancreatic B cells.

28
Q

What is cosecreted with insulin by the pancreatic B-cells?

A

C peptide

29
Q

Are C peptide levels high or low in patients with Diabetes Mellitus 1?

A

Low

30
Q

What is the clinical presentation of a patient with Type 1 DM?

A 
Polyuria
Polydipsia
Unintentional weight loss
Polyphagia
Often these patients present with DKA initially
31
Q

How do patients with Type 1 DM usually present initially?

A

in DKA

32
Q

What are the characteristics of DKA?

A

hyperglycemia
volume depletion
acidosis (increased anion-gap metabolic acidosis)

33
Q

What causes DKA?

A

Absolute deficiency of anabolic hormone insulin

34
Q

How do you treat patients in DKA?

A

Sodium-containing fluids (expand plasma volume)
Insulin (treat hypoglycemia)
Potassium (?)

35
Q

What is the primary defect in Type 2 DM

A

Insulin resistance: abnormal resistance of target tissues (muscle, adipose…) to circulating insulin.

36
Q

An increase in adipose tissue causes down-regulation of what?

A

Insulin receptor synthesis

37
Q

Why does DKA not usually occur in DM Type 2 patients?

A

The insulin that is present is capable of inhibiting hepatic ketogenesis but not abundant enough to prevent hyperglycemia

38
Q

What is hyperosmolar hyperglycemic nonketotic coma (HHNC), also known as hyperosmolar hypertonic syndrome (HHS)?

A

If diabetes is poorly managed or a major illness occurs, plasma glucose and plasma osmolarity may become pathologically elevated.
Caused by severe volume depletion from prolonged hyperglycemic diuresis.

39
Q

What are they sulfonylurea drugs?

A

Tolbutamide

Glyburide

40
Q

What is the primary hormone of the fasting state when thinking of glucose regulation?

A

Glucagon

41
Q

What is the primary stimulus for glucagon secretion from islet cells?

A

Amino acids, but also stimulated by low plasma glucose.

42
Q

At physiologic levels, glucagon primarily acts on what organ?

A

Liver.
Promotes hepatic glycogenolysis and gluconeogenesis.
Further stimulates B-oxidation of fats by liver for energy to support gluconeogenesis.

43
Q

What are the main functions of aldosterone?

A

Maintain intravascular volume and maintain arterial blood pressure and adequate organ perfusion.

44
Q

Where does aldosterone act? What metabolites are involved?

A

Kidneys. Stimulate sodium reabsorption, potassium secretion, and hydrogen ion secretion.

45
Q

What are the adrenal catecholamines? What a.a. are they synthesized from?

A

Epinephrine
Norepinephrine
Dopamine
Synthesized from tyrosine in the adrenal medulla

46
Q

The secretion of Epinephrine by the adrenal medulla is under the control of what system?

A

Autonomic Nervous System

47
Q

The endocrine regulation of calcium depends on the actions of what two hormones?

A

PTH
Calcitriol (active Vitamin D)

Calcitonin contributes minimally to calcium homeostasis

48
Q

Where is most calcium found?

A

Bone.

49
Q

In hypoalbuminemia, total plasma calcium levels are increased/decreased/same and ionized calcium levels are increased/decreased/same?

A

Total calcium levels decreased

Ionized free calcium are normal

50
Q

Hypocalcemia will lead to what sort of manifestations?

A

Enhanced membrane excitability –> muscle spasms (tetany), cardiac arrhythmias, seizures.

51
Q

Hypercalcemia leads to what sort of manifestations?

A

It reduces membrane excitability, leading to muscle weakness and stupor.

52
Q

What are some causes of hypercalcemia?

A 
Primary hyperparathyroidism
Hypercalcemia of malignancy
Milk-alkali syndrome
Granulomatous Disease (TB and sarcoidosis)
Lymphoma
Paraneoplastic syndromes
Vitamin D toxicity
Familial Hypocalciuric Hypercalcemia
53
Q

What cells release PTH?

A

parathyroid chief cells in response to hypocalcemia or hyperphosphatemia.

54
Q

calcitriol chemical name

A

1,25-dihydroxyvitamin D3

This is the active form of vitamin D

55
Q

Clinical description of hyperparathyroidism:

How does that saying go…?

A

Stones, bones, grones and psychological overtones.

56
Q

Calcidiol (25-hydroxyvitamin D) must be converted to its active form _____ in the _____

A

calcitriol; kidneys

57
Q

PTH stimulates the synthesis of _______ in the kidneys by increasing the synthesis of the enzyme ________ in the proximal tubules.

A

calcitriol; 1alpha-hydroxylase

58
Q

How does calcitriol affect calcium homeostasis?

A

Stimulates calcium and phosphate absorption in the intestine

59
Q

PTH and calcitriol act on stromal cells and osteoblasts to produce ______. In turn, this molecule will interact with its receptors on mononuclear progenitors of the monocyte-macrophage family, causing them to fuse together and become multinucleated cells known as osteoclasts.

A

RANKL

ENDOREPRO MODULE (11 decks)

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