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Renal > Renal Physiology VII > Flashcards

Renal Physiology VII Flashcards

1
Q

Since the ability of the liver to respond to insulin is impaired, hepatic gluconeogenesis is upregulated, setting in motion a viscious cycle of

A

Hyperglycemia and hyperinsulinemia

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2
Q

Obesity is defined as a body mass index (BMI) of

A

Greater than 30kg.m^2

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3
Q

The deposition of fat in the regions of the hip and buttocks is not strongly correlated with

A

Metabolic disease

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4
Q

Whereas accumulation of visceral fat is linked with a syndrome that is described as

A

Type 2 DM

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5
Q

The distribution of fat around the abdominal wall and visceral mesenteric location

A

Android obesity

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6
Q

On the other hand, the presence of subcutaneous abdominal fat has less of an association with

A

Insulin resistance

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7
Q

Correlated with the development of hypertension and dyslipidemia, among other risk factors for cardiovascular disease

A

Android obesity

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8
Q

The android obesity phenotype results in an abnormally increased

A

Waist-to-hip tatio (greater than 0.9 in males and 0.85 in females)

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9
Q

Has a gene expression pattern that makes it distinct from other fat stores

A

Visceral fat

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10
Q

Mutations and/or abnormal expression/activity of adipokines (e.g., adiponectin and leptin), cytokines (e.g., tumor necrosis factor-a, TNFa), and FFA which are produced by visceral fat have the ability to alter both

A

Glucose metabolism and Insulin sensitivity

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11
Q

Each increae sensitivity to insulin

A

Leptin and adiponectin

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12
Q

Has been shown to impede insulin dependent glucose metabolism

A

TNFa

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13
Q

Impede both insulin secretion and insulin-directed glucose uptake in peripheral tissues

A

FFAs

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14
Q

FFAs stimulate dipocytes to secrete

A

TNFa

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15
Q

TNFa in turn exerts positive feedback on

A

FFA secretion

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16
Q

In response to insulin resistance, visceral fat undergoes

A

Lipolysis

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17
Q

The lypolysis that visceral fat undergoes results in increased levels of

A

Tryglycerides and small and dense LDL (the really bad kind of LDL) and decreased HDL

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18
Q

Visceral fat thus increases

A

CV risk

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19
Q

It is therefore important to realize that visceral abdominal fat is very active in terms of its production of a cohort of factors which

A

Impede insulin secretion and impair insulin-dependent glucose uptake

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20
Q

The ideal goals for preventing the progression of IGT to Type 2 DM

A

Weight loss and exercise

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21
Q

A biguanide that impairs hepatic gluconeogenisis and intestinal glucose absorption, and enhances peripheral glucose uptake

A

Metformin

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22
Q

An insulin sensitizer

A

Thiazolideniones (pioglitazone)

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23
Q

Insulin secretagogues that promote endogenous insulin production

A

Sulfonylureas

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24
Q

Injectables or insulin pump that can replace pancreatic and islet cells

A

Insulin replacement

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25
Q

Impedes glucose reabsorption from forming urine

A

SGLT2 inhibitors

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26
Q

Impede the degradation of glucagon-like peptide 1 (GLP-1)

A

DPP-4 inhibitors

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27
Q

Promotes insulin secretion and inhibits glucagon secretion

A

GLP-1

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28
Q

The renal system is an important contributer to

A

Glucose counter regulation

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29
Q

What do the kidneys use for gluconeogenesis?

A
  1. ) LActate (predominant)
  2. ) Glutamine
  3. ) Glycerol
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30
Q

Under conditions of prolonged fasting, hypoglycemia, and acidosis, the kindeys can account for what percentage of gluconeogenesis?

A

As much as 20%

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31
Q

Glucagon, glucocorticoids, and norepinephrine/epinephrine all stimulate

A

Renal gluconeogenesis

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32
Q

Following hepatic failure, the kidneys can partially compensate for

A

Impaired gluconeogenesis

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33
Q

Renal glucose uptake is regulated by

A

Insulin

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34
Q

The kidneys also metabolize insulin in order to lower

A

Plasma insulin levels

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35
Q

This partially explains the hypoglycemia that is often observed as a result of

A

Renal failure

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36
Q

Within the nephron, glucose is freely filtered and reabsorbed with reabsorption being approximately equal to

A

Filtration

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37
Q

Reabsorbs essentially ALL of the filtered glucose

A

The proximal tubule

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38
Q

The reabsorption of glucose by the proximal tubule is mediated by the regional expression of :

  1. ) Apical?
  2. ) Basolateral?
A
  1. ) SGLT1 and SGLT2

2. ) GLUT1 and GLUT2

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39
Q

An Na+-glucose cotransporter that is driven by Na+ gradients established by the Na+/K+ ATPase

A

SGLT

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40
Q

Functions via facilitated diffusion

A

GLUT

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41
Q

The threshold for spillover of glucose into the excreted urine is approximately

A

180 mg/dL plasma

42
Q

1dL =

A

100 mL

43
Q

Physiologic glucose levels are between

A

65 (fasting) to 120 (post prandial)

44
Q

In the diabetic, failure of the insulin system results in impaired

A

Cellular glucose uptake

45
Q

This results in a marked increase in

A

Serum glucose

46
Q

As a result, the filtered load of glucose goes through the roof. When the reabsorptive machinery within the tubule becomes saturated (180 mg/dL) the result is

A

Glucosuria

47
Q

The primary diagnosis for approximately 30-40% of end stage renal diseases (ESRD)

A

Diabetes melitus

48
Q

Approximately 1/3 of patients with diabetes develop

A

Microalbuminuria (elevated urine albumin)

49
Q

This process of microalbuminuria often precurses

A

Proteinuria (macroalbuminuria), diabetic neuropathy, and renal fucntion loss

50
Q

Proteinuria due to a loss in glomerular function

A

Glomerular proteinuria

51
Q

Determined by the following: the mean transcapillary

hydraulic pressure difference, glomerular surface area, and the size- and charge-selectivity of the glomerular membrane

A

Glomerular proteinuria

52
Q

How much albumin per day is typically filtered and completely reabsorbed by the glomeruli?

A

1g albumin

53
Q

Microalbuminuria in diabetics is predictive of a high probability of

A

Cardiovascular morbidity and mortality as well as progressive renal disease

54
Q

Functions as an antigen which causes immune and cellular responses within the nephron

-the form of albumin in diabetics

A

Glycated albumin (glycosylated albumin)

55
Q

Causes the generation of reactive oxygen species which can chelate proteins and cause other damage to the glomerular embrane

A

Glycated albumin

56
Q

In the face of the assault by glycated albumin, the glomerular membrane loses

A

Size and charge selectivity

57
Q

Induce the 1) overloading of tubule intracellular lysosomes, 2) local production of inflammatory cytokines, and 3) increased synthesis of extracellular matrix proteins within the tubular tissues

A

Elevated concentrations of urinary proteins

58
Q

Collectively this leads to

A

Glomerulosclerosis, fibrosis, and renal failure

59
Q

During the early stages of diabetes, the glomerulus and tubular epithelium can

-correlated with thickening of cellular basement membranes

A

Hypertrophy

60
Q

This condition of glomerular hypertrophy is commonly accompanied by what 2 things?

A
  1. ) Supranormal GFR (hyperfiltration)

2. ) Microalbuminuria

61
Q

What three things induce unfavorable glomerular remodeling?

A
  1. ) Hypertension
  2. ) Hyperlipidemia
  3. ) Hyperglycemia
62
Q

Excess glucose in the glomerular filtrate (due to hyperglycemia) induces a significant upregulation in the expression of

A

Proximal tubule SGLT2

63
Q

Upregulation in the expression of proximal tubule SGLT2 enables increased proximal Na+ reabsorption, resulting in decreased Na+ delivery to the

A

Macula Densa

64
Q

The TGF mechanism is thus tricked into perceiving this as low perfusion and responds in kind with the secretion of

A

Vasodilators

65
Q

The vasodilators secreted by the TGF result in dilation of the

A

Afferent arteriole

66
Q

Afferent dilation results in

A

Increased glomerular pressure and hyperfiltration

67
Q

In addition, experimental evidence shows that inadequate glycemic regulation and diabetic hypertension collectively tax the vascular endothelium by

A

Pressure-induced capillary stretch

68
Q

This causes increased vascular permeability and leads to

A

Glomerular injury

69
Q

These conditions collectively support an amplifying cycle of increased reabsorption by the proximal tubule
and its stimulatory effect on

A

GFR

70
Q

From the vascular side, the diabetic kidney may receive aberrant signals regarding

A

ECF volume

71
Q

These miscued feedback loops can then induce an inappropriate response within the renal microvasculature that leads to a cycle of osmotic imbalances and increased tubule reabsorption, which once again

A

Stimulates GFR

72
Q

So-called tubular events can result in altered GFR due to disruptions in the

A

TGF mechanism

73
Q

These disrupted TGF mechanisms are at the root of a cascade of problems that disrupt the reabsorptive capacity of tubules upstream from the

A

Macula densa (so-called primary tubule events)

74
Q

Over time, glomerular basement membrane thickening, hypertrophy, podocyte injury/loss, and glomerulosclerosis develop, leading to

A

Decreased GFR

75
Q

The final common pathway to ESRD is the diabetic kidneys formation of

A

Tubulointerstitial fibrosis

76
Q

Unchecked extracellular glucose assaults

A

Renal interstitial and tubule cells

77
Q

This overwhelming glucose load stimulates the

A

RAS

78
Q

Promotes the release of intrarenal fibrogenic cytokines, chemokines, chemotactic factors, cell adhesion molecules, and growth factors; while inhibiting the production of antifibrogenic factors

A

RAS

79
Q

Collectively, this milieu facilitates the formation of glomerulosclerosis and may promote epithelial-to-mesenchymal cell transitions that lead to

A

Tubulointersitital Fibrosis

80
Q

Has been shown to induce phosphorylation of insulin receptor substrate-1 (IRS-1)

A

An-II

81
Q

This phosphorylation event blocks insulin from using IRS-1, which induces a state of

A

Insulin resistance

82
Q

In addition, upregulated RAS activity can impair the expression of

A

Nephrin

83
Q

A transmembrane protein that aids in restricting protein filtration across the glomerulus

-present within the slit diaphragms of glomerular podocytes

A

Nephrin

84
Q

Thus, in the face of a sustained RAS challenge, nephrin content is compromised, resulting in a

A

Leaky glomerulus

85
Q

Recall, AII stimulates aldosterone secretion. Elevated aldosterone means increased Na+ retention, Na+ retention means increased H2O retention, and H2O retention means elevated BP and the propensity for

A

Diabetic hypertension

86
Q

Have been shown to reduce proteinuria and slow the progression of diabetic neuropathies in some diabetic patients

A

Treatment with renin and ACE inhibitors and ARBs

87
Q

Furthermore, in certain patients with diabetic neuropathies, treatment with renin and ACE inhibitors and ARBs togehter provides a greater renoprotective effect than

A

Treatment with just one

88
Q

Hyperglycemia can induce

-will make diabetic ketoacidosis more complicated

A

Hyperosmolality

89
Q

Hyperosmolality will induce osmotic diuresis, resulting in a continuous siphoning off of

A

Intracellular K+

90
Q

This siphoning of intracellular K+ an result in

A

Hyperkalemia

91
Q

Furthermore, hyperkalemia with volume depletion (i.e. due to the osmotic diuresis) will stimulate

-will exacerbate the loss in total body K+

A

Aldosterone secretion

92
Q

It is not unusual for the DKA patient at the time of presentation to have eu- or hyperkalemia in the face of

A

Depleted total body K+

93
Q

What is the key component in the treatment of DKA?

A

Insulin therapy

94
Q

Remember that the most sensitive response to insulin is not cellular glucose uptake, but rather

A

Cellular K+ uptake

95
Q

Plasma K+ levels generally fall with

A

Insulin therapy

96
Q

The majority of Ca2+ and phosphorus that is reabsorbed is reabsorbed in the

A

Proximal tubule

97
Q

Coupled to Na+ reabsorption within the proximal tubule and is also orchestrated by parathyroid hormone (PTH) and diuretics elsewhere in the nephron

A

The regulation of Ca2+ and PO4 reabsorption

98
Q

Changes in serum calcium content signal the parathyroid glands to

A

Increase PTH secretion when Ca2+ is low and vice versa

99
Q

Kidney tubular cells contain specific enzymes which hydroxylate 25-hydroxy vitamin D (calcidiol) to form

A

1, 25-dihydroxyl vitamin D (Calcitriol)

100
Q

The formation of calcitriol is primarily stimulated by

A

PTH and hypophosphatemia

Renal (10 decks)

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