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Renal > Renal Physiology VI > Flashcards

Renal Physiology VI Flashcards

1
Q

Reabsorbed urea assists in maintaining the hyperosmotic gradient that exists within the

A

Renal medullary interstitium

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2
Q

This gradient aids in the formation of concentrated urine, and, medullary urea concentrations ensure that the majority of the filtered load of urea is trapped within the kidneys for

A

Eventual Elimination

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3
Q

Like the other filtered solutes, lots of urea (approximately 50%) is reabsorbed from the

A

Proximal tubule

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4
Q

Within the thin descending and ascending limbs, urea is secreted via the

A

UT2 facilitated transporter

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5
Q

This removes a lot of urea from the interstitium, and because of this, in the collecting tubules the lumenal [urea] approximates

A

110% of its filtered load

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6
Q

In order to prevent excess washing-out of the medullary interstitium, urea is then reabsorbed from the medullary collecting ducts and back into the renal medullary interstitium; this process is mediated by

A

UT1 and UT4 facilitated transporters

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7
Q

This whole process describes

A

Renal urea cycling

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8
Q

Renal urea cycling, along with Na+, supports the hypertonicity of the medullary intersitium that promotes the

A

Reabsorption of H2O from forming urine

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9
Q

In a healthy person, fasting plasma glucose falls within the range of approximately

A

75-115 mg/dl

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10
Q

In a healthy person, a two-hour post prandial plasma glucose should not exceed

A

120 mg/dL

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11
Q

Abnormal elevations in these values indicate the presence of a disorder of carbohydrate metabolism such as

A

Diabetes Mellitus

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12
Q

Glucagon, epinephrine, cortisol, and GH each increase

A

PLasma Glucose

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13
Q

Lowers plasma glucose

A

Insulin

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14
Q

Glucagon, epinephrine, cortisol, GH, and insulin control plasma glucose by which mechanisms?

A
  1. ) Breakdown/formation of glycogen
  2. ) Adipogenesis
  3. ) Absorption of dietary glucose in GI system
  4. ) Synthesis of glucose
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15
Q

The process of glucose uptake and storage as glycogen

A

Glycogenesis

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16
Q

The metabolism of glycogen to yield glucose

A

Glycogenolysis

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17
Q

The synthesis of glucose from other substrates

A

Gluconeogenesis

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18
Q

Functionally divided into digestive (exocrine) and endocrine segments because of its dual function

A

The Pancreas

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19
Q

The pancreas is comprised of which two major types of tissue?

A
  1. ) Acini glands (exocrine)

2. ) Islets of Langerhans (endocrine)

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20
Q

The Islets of Langerhans contain three populations of endocrine cells with distinct functions. What are they?

A

alpha cells, beta cells, and delta cells

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21
Q

Secrete glucagon

A

Pancreatic alpha cells

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22
Q

Secrete insulin

A

Pancreatic Beta cells

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23
Q

Secrete somatostatin

A

Pancreatic delta cells

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24
Q

Insulin is synthesized within

A

Pancreatic beta cells

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25
Q

Under normal circumstances, insulin is secreted when serum glucose levels exceed approximately

A

100 mg/dL

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26
Q

Insulin is a storage hormone in that is promotes

A

Glycogenesis and lipogenesis

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27
Q

Insulin together with GH promotes

A

Muscle anabolism

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28
Q

Promotes the cellular uptake of serum glucose in the liver, skeletal muscle, and fat

A

Insulin

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29
Q

Thus, when serum glucose levels rise, insulin production and secretion is

A

Stimulated

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30
Q

Insulin blocks

A

Liver gluconeogenesis

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31
Q

Cellular uptake of both K+ and FFA are stimulated by

A

Insulin

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32
Q

A specific transport protein located within the plasma membrane of B cells that facilitates the movement of glucose into the B cells

A

Glucose transporter-2 (GLUT-2)

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33
Q

Within the B cells, glucose is phosphorylated by glucokinase, and this results in the formation of

A

Glucose-6-phosphate (G-6-P)

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34
Q

Intracellular ATP concentrations rise and ATP-sensitive K+ channels are phosphorylated in response ot the formation of

A

G-6-P

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35
Q

This causes closure of the ATP-sensitive K+ channels resulting in

A

Cell depolarization

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36
Q

Depolarization causes voltage-gated Ca2+ channels to open. The subsequent elevation in intracellular Ca2+ activates the

A

Secretory granule machinery

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37
Q

Circulates in bioactive form and activates it’s specific cell surface receptor in target cells

A

Insulin

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38
Q

Activation of insulin is coupled to the activation of glucose carrier proteins which results in the

A

Rapid influx of glucose by facilitated diffusion

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39
Q

Insulin promotes the uptake, storage, and utilization of glucose by the

A

Liver

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40
Q

Insulin also inhibits liver

A

Gluconeogeneis and glycogenolysis

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41
Q

The predominant source of sustaining blood glucose during fasting periods via gluconeogenesis and glycogenolysis

A

Liver

42
Q

Begins with the diffusion of glucose into hepatic cells

A

Glycogenesis

43
Q

Once in the cells, glucose is rapidly phosphorylated by glucokinase, thus forming

A

G-6-P

44
Q

The conversion of glucose into G-6-P is important because G-6-P can not

A

LEve the cells

45
Q

Serves as the intermediate that can be further metabolized for glycogen synthesis

A

G-6-P

46
Q

Additionally, G-6-P serves as an entry intermediate into biochemical pathways that enable the production of

A

ATP

47
Q

In addition to being expressed with hepatocytes, glucokinase is produced within

A

Pancreatic B cells

48
Q

Glucose dependent glucokinase activity mediates the secretion of

A

Insulin

49
Q

The major site of post prandial glucose disposal

A

Skeletal muscle

50
Q

Provides the substrate for the production of ATP in skeletal muscle

A

Glucose

51
Q

Uses glucose (from glycogen stores) and FFA for the production of the vast quantities of ATP that are needed to sustain cross-bridge cycling

A

Metabolically active skeletal muscle

52
Q

Activated in response to increased metabolic demand in order to provide increased intracelular glucose for use in the production of ATP

A

Glycolytic pathway

53
Q

Insulin is the major hormone that stimulates the synthesis of

-to be stored in adipose tissue

A

Triglycerides

54
Q

In adipose tissue, promotes the use of glucose rather than fatty acids for metabolic energy

A

Insulin

55
Q

In the liver, insulin stimulates

A

Fatty acid synthesis

56
Q

In the liver, insulin augments the conversion of excess glucose into

A

Fatty acids

57
Q

In the liver, the synthesis of hepatic triglyceride and lipoprotein are increased in the presence of

A

Insulin

58
Q

In skeletal muscle, Insulin suppresses the activity of

-Blocks oxidation of FFAs

A

Lipoprotein lipase

59
Q

An anabolic hormone and much of it’s anabolic affect is attributed to it’s effects on protein metabolism, especially in the presence of GH

A

Insulin

60
Q

For example, insulin increases the uptake of certain aminos into muscle cells and also can stimulate

A

Translation

61
Q

Concomitantly, the catabolism of certain muscle proteins is impaired by

A

Insulin

62
Q

What occurs in the absence of insulin from amuscular standpoint?

A

Increased catabolism, decreased protein synthesis

63
Q

Insulin secretion declines precipitously when serum glucose levels are

A

Less than 80-90 mg/dL (i.e. normal fasting concentration)

64
Q

Thus, when serum glucose is low, insulin secretion is suppressed and for tissues get their energy from

A

Fat metabolism

65
Q

A large polypeptide that is secreted by the alpha cells within the islets of Langerhans

A

Glucagon

66
Q

Referred to as the hyperglycemic hormone because it induces rapid elevations in serum glucose levels

A

Glucagon

67
Q

Glucagon is thought to act exclusively in the

A

Liver

68
Q

Within hepatocytes, glucagon stimulates

A

Glycogenolysis and gluconeogenesis

69
Q

The pattern for glucagon secretion is inversely proportional to

A

Serum insulin and glucose levels

70
Q

Glucagon secretion increases during a fast, when serum glucose levels are below

A

80-90 mg/dL

71
Q

Glucagon is especially important in

A

Neonates

72
Q

Aids in maintaining the proper level of serum glucose and avoiding extremes in hypoglycemia while babies are learning to break down and extract sugars and other nutrients from milk or formula

A

GLucagon

73
Q

A polypeptide secreted by the delta cells within the islets of Langerhans

A

Somatostatin

74
Q

In general, levels of somatostatin increase during the

A

Post-prandial period

75
Q

Exerts transitory inhibitory effects on insulin and glucagon secretion

A

Somatostatin

76
Q

A disturbance in the normal carbohydrate metabolism that results from insulin insufficiency

A

Diabetes Mellitus

77
Q

If a patient has a fasting glucose level of higher than 126 mg/dL on 2 occasions, and/oral oral glucose tolerance test greater than 200 mg/dL at two hours on two occasions and or HbA1c gretaer than 6.5 % is classified as

A

Diabetes Mellitus (DM)

78
Q

DM is classified as an HbA1c level of greater than

A

6.5%

79
Q

HbA1c is essentially just Hb with a

A

Glucose tacked on

80
Q

A good indication of glycemic status of a patient within the preceding 8-12 weeks

A

HbA1c

81
Q

Diabetes Mellitus has which three main smyptoms?

A

The three Ps

  1. ) Polydipsia (thirsty)
  2. ) Polyuria (peeing a lot)
  3. ) Polyphagia (ecessive hunger)
82
Q

Since hyperglycemia increases the filtered load of glucose, more glucose in the forming urine acts as an

A

Osmotic diuretic (thus polyuria)

83
Q

Other common sequelae of DM result from complications of microvascular and macrovascular pathology as the disease progresses. These include

A

Blurred vision, paresthesias, muscle fatigue, and muscle cramps

84
Q

With severe enough impaired glucose uptake, metabolic demand (i.e. ATP production) cannot be met by glycolysis so instead metabolism shifts from glycolysis to lipolysis resulting in the oxidation of free fatty acids and the formation of

A

Ketone bodies

85
Q

Keep in mind that ketoacids in and of themselves are not all bad, they do provide a substrate for

A

Energy

86
Q

However, when ketoacid production exceeds that of usage, the accumulation of these acids results in the development of a ketoacidosis known as

A

Diabetic Ketoacidosis

87
Q

The broad clinical markers of type 1 DM are

A

Hypoinsulinemia with hyperglycemia

88
Q

Type 1 DM is calssified as an

A

Autoimmune disorder

89
Q

What are the two subtypes of type 1 DM?

A

Type 1A and type 1B

90
Q

Autoimmune in nature and results from the degeneration of pancreatic B cells or the suppression of B cell function due to infiltration by mononuclear/lymphocytic cells

A

Type 1A DM

91
Q

Known as idiopathic non-autoimmune diabetes

-less common

A

Type 1B DM

92
Q

Type 1 DM is medically managed by

A

Insulin replacement

93
Q

The most predominant form of DM, accounting for approximately 90% of DM

A

Type 2 DM

94
Q

Insulin resistance appears to precurse the development of impaired glucose tolerance, but rarely progresses to Type 2 DM without some decrement in

A

B cell function

95
Q

Predicts the progression from impaired glucose tolerance (IGT) to full on type 2 DM

A

Elevated FFA

96
Q

In fact, the effect of insulin on cellular FFA uptake is more profound than its effect on

A

Glucose uptake

97
Q

What has a more predominant genetic component, type 1 DM or type 2 DM?

A

Type 2

98
Q

results from some defect most likely at the level of the insulin receptor, insulin transport, and/or insulindependent signal transduction, with resultant tissue insensitivity to insulin

A

Type 2 DM

99
Q

Type 2 DM is defined by

A

Insulin insensitivity

100
Q

Therefore, type 2 is polygenic in nature with combinations in

A

Insulin resistance and Insulin secretion

101
Q

Manifests in the major insulin-sensitive tissues, those being skeletal muscle, fat, and to some degree the liver

A

Insulin resistance

102
Q

Because the target cells can not effectively respond to insulin, serum insulin levels may be normal or more likely elevated in the face of

A

Hyperglycemia

Renal (10 decks)

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