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N361: Pathophysiology II > Module 12 - Renal Failure > Flashcards

Module 12 - Renal Failure Flashcards

1
Q

Renal Medulla

A

Inner part of the kidney made of renal pyramids and tubular structures

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2
Q

Renal Cortex

A

Outer layer of the kidney

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3
Q

Renal Artery

A

supplies blood to the kidney

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4
Q

Renal Pyramid

A

channels output to renal pelvis for excretion

this is where the collecting ducts come together

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5
Q

Renal Calyx

A

channels connecting the renal pyramids to the renal pelvis

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6
Q

Renal Vein

A

about 99% of filtered blood is circulated through this vein

1% contains waste products and undergoes further processing

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7
Q

Renal Pelvis

A

Blood containing waste products forms urine here and is channeled away

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8
Q

Ureter

A

tube that terminates in the urethra

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9
Q

A lot of blood exchange happening in the kidneys occurs at …

A

the distal and proximal tubules (they help maintain acid base, fluid and electrolyte balances)

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10
Q

Both the distal and proximal tubules are involved in ___

A

reabsorption

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11
Q

Along with reabsorption, the distal tubule is involved in ___

A

excretion

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12
Q

Filtrate

A

the filtering fluid in the kidneys until nothing else is removed in which is becomes urine and is excreted

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13
Q

Parenchymal Tissue of the Kidney

A

Nephron

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14
Q

___ flow goes to the nephron

A

Arteriole

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15
Q

Afferent Arteriole

A

carries arteriole blood toward the Bowman’s Capsule

hydrostatic pressure going into the glomerulus

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16
Q

Efferent Arteriole

A

Carries arteriole blood away from the Bowman’s Capsule

hydrostatic pressure coming out of the glomerulus

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17
Q

What controls arteriole flow

A

pressure

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18
Q

Bowman’s Capsule

A

capsule surrounding the filter of the kidney, the Glomerulus

contains the glomerulus and acts as a filter for the urine/filtrate

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19
Q

Glomerulus

A

the filter of the kidney

A network of twisted capillaries acting as a filter for the passage of protein free and RBC free filtrate

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20
Q

What is abnormal to see go through the Bowmans capsule and why?

A

Normally in health, proteins and RBCs are too large to get through the bowman’s capsule - if proteins or RBC are in urine than that is abnormal

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21
Q

What is the pathway to through the nephron

A

Afferent Arteriole –> Bowmans Capsule and Glomerulus –> Proximal Convoluted Tubule –> Loop of Henle –> Distal Convoluted Tubule –> Collecting duct –> renal pyramids –> ureters –> Bladder –> Urethra and exit

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22
Q

Medullary Nephrons

A

Nephrons that go deeper into the kidney

since they are deeper they have greater urine concentrating ability, but will be damaged sooner

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23
Q

Cortical Nephrons

A

more shallow nephrons with lower concentrating ability

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24
Q

Why are Medullary nephrons injured before cortical ones?

A

Because of impaired/compromised blood flow

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25
Q

The deeper the medullary nephron goes…

A

the greater the ability to concentrate urine - but also the first to be damaged

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26
Q

Concentrating gradients of the kidney..

A

increase as you go from the cortex to the inner most layer

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27
Q

Proximal Convoluted Tubule (PCT)

A

Site of reabsorption of glucose, AA, metabolites, and electrolytes from filtrate

Reabsorbed substances returned to circulation

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28
Q

Loop of Henle

A

A U Shaped section of the nephron tubule located in the medulla

Extends from the PCT to the DCT

site for further concentration of filtrate through reabsorption

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29
Q

Distal Convoluted Tubule (DCT)

A

site from which filtrate enters the collecting tubules

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30
Q

Collecting Tubules/Ducts

A

Releases urine to the ureter

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31
Q

What does glucose do in the kidney in health

A

it will be reabsorbed, it is a small molecule that can pass through, but the body wants and gets it back

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32
Q

What area of the nephron reabsorbs glucose and other small substances?

A

PCT

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33
Q

Glucose in the urine is ___

A

abnormal

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34
Q

The concentrating mechanism of the nephron is …

A

the loop of Henle

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35
Q

What happens if you lose the loop of Henle?

A

You cannot concentrate filtrate/urine - isosthenuria

Nocturia will also occur

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36
Q

Isosthenuria

A

urine with the same concentration as the blood

this is d/t damage to the loop of Henle which is unable to reabsorb anything and concentrate the urine

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37
Q

What is one of the first signs of kidney damage

A

Nocturia - getting up a lot at night since more urine is made and not concentrated

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38
Q

What area of the nephron has acid base balance occur due to bicarbonate?

A

DCT

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39
Q

What area of the kidney does not have concentration occur?

A

DCT

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40
Q

In the kidney, Vascular pressure means…

A

hydrostatic pressure (push)

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41
Q

Ureters

A

16-18” muscular tubes that contract rhythmically to transport urine from each kidney to the bladder

tubes

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42
Q

Urinary Bladder

A

sac with muscular walls that collects and holds urine that is expelled from the ureters every few seconds

storage

detrusor muscle wall

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43
Q

Urethra

A

narrow tube leading out of the body through which urine is expelled from the bladder

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44
Q

In the nephron the fluid is ___, but you excrete ___

A

filtrate; urine

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45
Q

The kidney makes urine in __

A

drops

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46
Q

3 Steps of Waste Collection and Elimination in the Kidney

A
  1. Glomerular Filtration
  2. Tubular Reabsorption
  3. Tubular Secretion
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47
Q

Glomerular Filtration

A

Filtering the blood that flows through the kidney’s blood vessels, or glomeruli

It is like spraying water through a T shirt with only small things getting through, nothing large - but what filters depends on intactness of membrane and pressure applied!

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48
Q

Tubular Reabsorption

A

reabsorbing filtered fluid through the minute canals (tubules) that make up the kidney

Products going back to the body from the filtrate to the blood

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49
Q

Tubular Secretion

A

Release of filtered substances by the tubules

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50
Q

How are secretion and excretion different?

A

Secretion is moving things from one place in the body to another place in the body - like K into Urine

Excretion is moving things from inside the body to outside the body - like urinating

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51
Q

Tubular Reabsorption and Secretion/Excretion occur where?

A

In the PCT and DCT (both of them)

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52
Q

What kind of processes are reabsorption, secretion, and excretion

A

they can be active processes needing energy or a co transporter, OR they can be a passive process with a concentration gradient

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53
Q

What are the basic functions of the kidneys?

A
  1. Water, electrolyte, and acid base HOMEOSTAWSIS
  2. Excretion of nitrogenous metabolic waste products: urea, uric acid, and creatinine
  3. Detoxifying drugs, toxins, and their metabolites
  4. Endocrine regulation of ECF volume and blood pressure: RAA and ADH
  5. Secretion of erythropoietin to simulate RBC production
  6. Endocrine control of calcium and phosphate metabolism: Activation of vitamin D and excretion of phosphates
  7. Catabolism of hormones like insulin, glucagon, parathyroid hormone, calcitonin, and GH
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54
Q

How can penicillin display the renal detoxification ability

A

Penicillin is actively secreted by the PCT so it is in an inactive form !

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55
Q

Aldosterone holds…

A

Sodium and water follows that

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56
Q

If you hold sodium…

A

you rid potassium

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57
Q

How is RAA activated

A

Low flow states activate sensors in the JGA near the glomerulus (so pressure or amounts of sodium) which causes RAA to get aldosterone to act on DCT (late part) and the collecting duct (where ADH works) as an osmoregulor

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58
Q

What is the end result of RAA/ADH

A

increased circulating volume in response to low pressure in the kidneys

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59
Q

Where does Aldosterone work

A

on the DCT (late part)

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60
Q

Where does ADH work

A

on the collecting duct

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61
Q

How is ADH activated

A

it is secreted in response to sensors in the hypothalamus

The posterior pituitary will release ADH to increase circulating water

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62
Q

ADH governs ___

A

water

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63
Q

When does the kidney release erythropoietin

A

release when there is low O2 to stimulate RBC production and maturation

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64
Q

Why does the kidney activate Vitamin D?

A

to have endocrine control of calcium and phosphate metabolism

it will control calcium maintenance and cause ridding of phosphates

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65
Q

Kidneys are __ organs

A

selfish organs

they can and will shut everything else down

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66
Q

Chronic Renal Failure Diagnostic Tests

A
  1. radiographs or ultrasound
  2. Serum abnormalities in BUN, creatinine, creatinine clearance, and GFR
  3. Low plasma pH
  4. Anemia
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67
Q

What can X Rays show us about the kidneys

A

can only show size, not much else

could show a small, atrophied kidney

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68
Q

What can ultrasounds tell us about the kidneys

A

they can show small, cystic lesions and also whether the kidneys are solid

can tell us about mass and fluids

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69
Q

BUN increases with what?

A
  1. Dehydration
  2. Renal Failure/Insufficiency
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70
Q

Is BUN a specific test that can diagnose renal failure?

A

No

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71
Q

What is a better indicator of renal failure diagnosis than BUN?

A

Creatinine

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72
Q

Elevated creatinine levels tell us…

A

about kidney dysfunction

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73
Q

What are the best 2 diagnostics for diagnosing renal failure

A
  1. Creatinine Clearance
  2. Glomerular Filtration Rate (GFR)
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74
Q

Why may low plasma pH tell us about kidney failure

A

It means the blood is acidic and there is a potential METABOLIC acidosis occurring

RR will be faster and deeper to blow off CO2 to compensate

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75
Q

How can Anemia tell us there is a renal issue

A

there is no erythropoietin secreted to make new RBC or mature RBC since the kidney is not working

Oxygenation can also be affected from free floating urea in the blood too

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76
Q

What is something else that can contribute to anemia regarding kidney failure other than Erythropoietin issues?

A

High concentrations of urea bathing the RBCs and making them not function as well or live as long

There is then less oxygenation

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77
Q

What may electrolyte levels look like on lab tests of diminished renal function?

A
  1. Na+ - normal or decreased
  2. Cl- - normal or decreased
  3. K+ - normal or increased
  4. CO2 (Bicarb) - Decrease
  5. Ca+2 - Decrease
  6. Phosphorus - Increase
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78
Q

Why may potassium levels be high or normal with renal issues? Why is this bad?

A

The kidney has problems ridding of potassium with insufficiencies

This is bad because K works on resting membrane potential and cardiac function and can cause issues there

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79
Q

Never give what without showing the kidneys are working first?

A

IV Potassium

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80
Q

Calcium and Phosphorus has a ___ relationship

A

inverse

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81
Q

Why is the relationship between calcium and phosphorus important in renal issues?

A

hyperphosphatemia and hypocalcemia can occur (which sets the threshold for heart cell firing usually)

this can cause rhythm disturbances or abnormalities

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82
Q

How can ABGs tell us about diminished renal function

A

There is metabolic acidosis with renal failure since bicarbonate is not reabsorbed to rid of acids

Also CO2 on a venous panel will be low representing bicarbonate and we may see RR rate changes to compensate

So, Bicarbonate levels would be low indicating renal issues

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83
Q

Why is BUN a poor indicator of renal function

A

It rises also in dehydration, GI bleeds, and renal failure

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84
Q

What is creatinine reabsorption usually like

A

It normally is not reabsorbed and is secreted by tubules

But this level will increase in renal failure

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85
Q

What other things are creatinine levels dependent on?

A

Renal Clearance

Muscle Mass (higher means higher creatinine)

Sex

Age (muscle masses)

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86
Q

Is creatinine a good indicator by itself?

A

While rising levels usually indicate RF, this is not a good indicator by itself

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87
Q

Normal BUN:Creatinine Ratio

A

1:10

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88
Q

What is a renal failure BUN:Creatinine Ratio

A

> 20:1

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89
Q

Azotemia

A

accumulation of nitrogenous waste in blood (urea, creatinine, others)

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90
Q

If you see azotemia, you know what?

A

There is likely renal failure from nitrogenous things gathering in blood

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91
Q

The best indicator of kidney function is …

A

Creatinine Clearance

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92
Q

Clearance

A

refers to the complete removal of a substance form the blood

it is the amount of blood that can be cleared in a specific amount of time — how long it takes for product to get out of the blood (time dependent)

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93
Q

Creatinine Clearance

A

volume of blood in mL that the kidneys can clear of creatinine in 1 minute

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94
Q

Why is Creatinine Clearance the most accurate measure of GFR

A

It acts as the most accurate measure of Glomerular filtration rate (GFR) since creatinine is filtered by the glomeruli but not reabsorbed by the tubules

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95
Q

Glomerular Filtration Rate (GFR)

A

the rate at which the glomeruli filter blood

its about 120 mL/minute (about half a can of soda every minute)

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96
Q

What is GFR a function of

A
  1. Permeability of the capillary walls
  2. vascular (hydrostatic) pressure
  3. Filtration Pressure
97
Q

What is the relationship between GFR and creatinine clearance?

A

direct relationship

since the tubules neither reabsorb nor secrete creatinine, the creatinine clearance = GFR

98
Q

If tubules did reabsorb creatinine, what would happen between creatinine clearance and GFR?

A

Clearance < GFR

99
Q

If tubules did secrete creatinine, what would happen between creatinine clearance and GFR

A

Clearance > GFR

100
Q

24 Hour Creatinine Clearance Test

A

You look at the level of creatinine in the urine and compare it to a venous blood draw of creatinine

101
Q

Gold standard for renal function is?

A

Creatinine clearance (and GFR)

102
Q

What kind of factors can impact creatinine clearance

A

age, weight, gender

103
Q

How does creatinine clearance differ between sexes?

A

Male - 1-2 gm/24 hours

Female 0.8-1.5 gm/24 hours

104
Q

GFR Male Estimate Formula

A

(140-Age)*(Weight in Kg) / (72 * serum creatinine in mg/dL)

105
Q

GFR Female Estimate Formula

A

(0.85) * Male Estimate

106
Q

Creatinine Clearance Formula

A

[GFR + (Quantity of urine) * (creatinine concentration in urine)] / serum creatinine

107
Q

The most accurate GFR is …

A

creatinine clearance

108
Q

How will a CBC look with renal failure

A

Decreased RBC and Hgb

Low Hct - 25-35% (Anephric 12-20%)

Microcytic Hypochromic Anemia

109
Q

Micocytic Hypochromic Anemia probably indicates what anemia?

A

Iron Deficiency Anemia

110
Q

Anephric

A

no kidney function

111
Q

How will serum proteins (albumin and globulin) alter with renal failure?

A

These plasma proteins which maintain oncotic pressure will be gone and the oncotic pressure will be missing meaning a lot of fluid enters interstitial spaces and stays there

This reflects the adequacy of protein intake

112
Q

What is the primary function of plasma proteins like albumin and globulin?

A

to hold fluid in the vascular space

113
Q

Why do renal patients need a strict diet of high biologic value protein?

A

The kidney cannot rid of metabolic waste during failure, when albumin is not being synthesized and is breaking down faster, so we need to have a healthy level but not too much as it can cause metabolic waste build up leading to toxicity

114
Q

Chronic Renal Failure

A

Progressive and irreversible destruction of the kidneys

115
Q

What is interesting about renal function and s/s of renal failure?

A

Until renal function is <50%, clinical manifestations are minimal as surviving nephrons take over the work of those lost

116
Q

What happens to the surviving nephrons when renal function is below 50%?

A

the surviving nephrons increase rate of filtration, reabsorption, and secretion –> Hypertrophy occurs with increased size and release of cellular contents -> more nephron progressively die and the rest have trouble handling demand –> Damage and eventual death of remaining nephrons

117
Q

What happens after the progressive loss of nephrons begins in renal failure?

A

Progressive loss of nephrons –> scar tissue forms –> renal blood flow reduced –> renin releases from low flow states –> Fluid overload and HTN

118
Q

Why does HTN as a result of the RAA system speed up renal failure?

A

HTN accelerates renal failure by increasing filtration and demand for reabsorption of plasma proteins (workload)

It also impacts the heart

119
Q

Causes for Chronic Renal failure

A

Chronic Glomerular Disease

Chronic Infections like chronic Pyelonephritis and Tuberculosis

Congenital Abnormalities like Polycystic Kidney Disease

Vascular Diseases like HTN or Nephrosclerosis

Obstructions like kidney stones

Collagen diseases like systemic lupus erythematous

Nephrotoxic agents like long term aminoglycoside therapy or Chemotherapy

Endocrine disorders like diabetic nephropathy

120
Q

Glomerulonephritis

A

Affects the capillaries in the glomeruli\

Occurs from inflammation from something like a strep infection

121
Q

Nephrosclerosis

A

Tons of nephron scarring

122
Q

Why can kidney stones cause renal failure?

A

The cause back pressure into the kidneys

123
Q

Aminoglycosides

A

an antibiotic that can be deadly to the kidney

124
Q

Stages of Chronic Renal Failure`

A
  1. Reduced Renal Reserve
  2. Renal Insufficiency
  3. Renal Failure (RF)
  4. End Stage Renal Disease (ESRD)
125
Q

What determines the stage of chronic renal failure?

A

GFR (which equals amount of creatinine cleared)

126
Q

Reduced Renal Deserve

A

first stage

GFR between 35-50% of the normal rate

Serum BUN and creatinine is normal

no symptoms of impaired renal function

this stage occurs because of the buffer from having 2 kidneys

127
Q

Renal Insufficiency

A

second stage

GFFR between 20-35% of the normal rate

Azotemia (Nitrogenous waste), Anemia (low RBC) , and HTN Begin

Early symptoms begin - isosthenuria, polyuria isotonic with plasma

128
Q

Renal failure

A

third stage

GFR less than 20-25% the normal rate

kidneys cannot regulate volume and solute composition –> decreased urine output –> edema, metabolic acidosis (no reabsorb bicarb), hypercalcemia

over uremia (urea and nitrogenous waste) –> neurologic, GI and CV complications

129
Q

End Stage Renal Disease (ESRD)

A

GFR less than 5% the normal rate

Atrophy and fibrosis in glomeruli and tubules

Dialysis or transplant needed for survival

no filtration ability left

130
Q

Why may renal patients be tired constantly

A

they get up constantly at night to pee

131
Q

Why do renal patients end up with pericarditis later one

A

irritation from urea (uremia)

132
Q

Uremic Syndrome

A

a complication of s/s of chronic renal failure includes:

lethargy, fits, coma

epistaxis

anemia

sallow pigmentation and pruritic excoriations

bruising

amenorrhea, impotence, infertility

myopathy

peripheral neuropathy

red eye

anorexia, N/V

HTN, pericarditis, heart failure

pleurisy

dyspnea on exercise

nail changes

bone pain

edema

red eye and frost

133
Q

Frost

A

crystallization of urine/uric acid on the brow in sweat

134
Q

Why is there epistaxis in uremic syndrome?

A

urea covers the RBCs and blood contents making platelet functioning less

this is the same reason renal patients get bruising

135
Q

What does Acidosis trigger?

A

the nausea center in the brain

136
Q

Why are renal patient’s skin so itchy

A

the uremia on the skin leaking through sweat

intense scratching episodes can cause taking of skin off and cause secondary infection

137
Q

How does the body function of body fluids change with renal disease

A

compensatory changes occur in tubular functions

decreased ability to synthesize ammonia and conserve bicarbonate occurs

Potassium cannot be excreted

cannot regulate sodium excretion

impaired ability to excrete phosphate

hyperphosphatemia and inability to activate vitamin D

138
Q

What are some of the manifestations of the body fluid changes in renal disease

A

fixed specific gravity of urine (isosthenuria)

metabolic acidosis

hyperkalemia

salt wasting or sodium retention

hyperphosphatemia

hypocalcemia and increased levels of PTH followed by hypercalcemia

139
Q

How can renal disease lead to hypercalcemia?

A

Hypocalcemia leads to signaling release of PTH from the parathyroid gland in order to increase calcium levels via absorption in the gut, activation of vitamin D in the kidneys, and increase reabsorption in DCT, and increase osteoclast activity

Since some of these are regulated by a failing kidney, the PTH must do most of the work to raise calcium and it continues since phosphorus cannot be rid of

this causes hypertrophy and sensitivity of vitamin D receptors leading to less sensitivity to Vitamin D and calcium levels by the parathyroid gland and thus continued release and increased PTH causing hypercalcemia

140
Q

How does the hematologic system get altered with renal failure?

A

impaired synthesis of erythropoietin and effects of uremia on blood (this means anemia occurs)

impaired platelet function (qualitative defect from uremia)

141
Q

Manifestations of the Renal failure related hematologic changes

A

Anemia

Bleeding tendencies

142
Q

What are the multi systemic effects of chronic renal failure via alterations in the hematologic system

A

Anemia - shortened lifespan of RBCs in toxic serum, decreased production of erythropoietin and inhibition of bone marrow, bleeding from coagulation defects (qualitative in PLTs), anticoagulation during dialysis may cause heavy menstrual and GI bleeding, and blood sampling during dialysis, loss of blood d/t machine, and dialyzer malfunction can occur

Immune responsiveness is also depressed making them susceptible to infection

143
Q

Treatment for the Hematologic Changes from CRF

A
  1. Epogen
  2. Dialysis to remove uremic toxins
  3. Transfusions - conservative administration
  4. Risk of excess Fe and K occur so treatment with chelating agents
144
Q

Epogen

A

synthetic erythropoietin

given SQ 3x a week (very expensive)

145
Q

What occurs as a result of renal treatment

A

racking up a lot of expenses

so they have separate coverage under their insurance plans and also have state programs to help

146
Q

Why are transfusions given to CRF patients?

A

It is given to them to make up for the bleeding that occurs d./t bad clotting

147
Q

Why are blood transfusions a conservative treatment for CRF?

A

Depresses function of normal bone marrow

Doing so decreases hepatitis risk

Potential for iron overload since blood breakdown from uremia releases iron that is stored

148
Q

Why are CRF patients given chelating agents?

A

Hyperkalemia from lysing of cells in the dialyzer and transfusions breaking cells

High iron from transfusions and RBC breakdown

149
Q

What alterations occur from CRF in the cardiovascular system

A

Activation of RAA mechanisms causing increases in vascular volume

Fluid retention and hypoalbuminemia

Excess ECF and anemia

Increased metabolic wastes in blood

150
Q

Manifestations of the Cardiovascular changes from CRF

A

HTN

Edema

CHF and Pulmonary Edema

Uremic Pericarditis

151
Q

____ is a potent vasoconstrictor

A

Angiotensin II

152
Q

Why do cellular and interstitial edema co occur in CRF?

A

there is fluid retention causing cellular edema and then there is interstitial edema from hypoalbuminemia

This hypoalbuminemia occurs relatively to fluid retention decreasing oncotic pressure, but there is also albumin loss in liver disease

153
Q

How can CRF lead to CHF

A

Workload and Anemia!

fluid retention gives a higher preload with HTN giving a higher afterload –> increased heart workload

Heart tissue is bathed in urea –> depressed pumping ability and RBC are not delivering oxygen like they should

This all leads to pulmonary edema and CHF

154
Q

Often CRF goes alongside ___ making dialysis tricky

A

CHF

155
Q

What are the multi system effects alterations in the cardiovascular system from CRF cause

A

HTN

Pericarditis r/t uremic effects and clotting defects

Myocardium issues

Hyperkalemia

156
Q

What is another potent vasoconstrictor beside angiotensin II

A

ADH

157
Q

Why does HTN occur in CRF

A

fluid overload from RAA and ADH functioning autonomously and being uncontrolled

158
Q

How does renal ischemia lead to CHF

A

renail ischemia –> RAA –> Vasoconstriction –> HTN –> LVH –> CHF

159
Q

What causes Hypertensive encephalopathy and what does it cause as a result?

A

high BP and excess blood volume cause HTN Encephalopathy

Increases ICP

HA

Retinal Changes

Seizure

Coma

CVAs

160
Q

What are the two leading causes of eye disease and retinal changes?

A

Increased ICP

Diabetes

161
Q

What can pericarditis r/t uremic effects and clotting defects from CRF lead to?

A

Pericardial Effusion

Cardiac Tamponade

162
Q

Cardiac Tamponade

A

heart failure from a right sided problem like pericardial effusion that does not let the heart fill and pump

163
Q

Why can high phosphorus hurt the heart?

A

High phosphorus will come back down by combining with calcium but then the body will put it in valves and other areas around the heart leading to dysfunction

If Calcium is low, PTH will pull it from bone to combine it but they then need to be placed in soft tissue and not bone

164
Q

What can cause the Hyperkalemia in CRF

A

Dietary Indiscretion (high K foods)

Increased Catabolism of cells

Decreased K secretion

Blood transfusions

Surgery

Acidosis from ion shifting (H in causes K out)

165
Q

Why are dietary restrictions on potassium so important in CRF

A

K is functional in resting membrane potential and a high level causes a higher potential and vice versa

this can lead to arrhythmias like Ventricular fibrillation that can cause death

166
Q

What are some EKG changes seen with hyperkalemia?

A

change sin conductivity and repolarization

prolonged PR

widened QRS

high peak T waves

167
Q

What is a common way CRF patients end up comiting suicide

A

excessive potassium intake

168
Q

What alterations in the GI system occur from CRF

A

increased metabolic wastes

decreased platelet function and increased gastric acid secretion from hyperparathyroidism

169
Q

What are the manifestations in the GI changes from CRF

A

Anorexia & N/V from metabolic wastes

GI Bleeding from decreased platelet function and hyperparathyroidism

170
Q

Other than calcium release, what else does PTH cause excess release of

A

Gastric Acids

171
Q

What alterations in the neurologic system occur from CRF

A

fluid and electrolyte imbalances

increases in metabolic acids and other small, diffusible particles such as urea

172
Q

What are the manifestations of the neurologic alterations from CHF

A

HA (F&E imbalances)

S/S of Uremic Encephalopathy (toxicity of brain tissue from urea)

S/S of neuropathy

173
Q

What are the signs and symptoms of uremic encephalopathy

A

lethargy

decreased alertness

loss of recent memory

delirium

coma

seizures

asterixis

muscle twitching

tremulousness

174
Q

Asterixis

A

twitching and tremors associated with liver disease

“Liver flapping”

175
Q

S/S of Neuropathy

A

restless leg syndrome

paresthesia

muscle weakness

paralysis

176
Q

Primarily all Neurologic effects from CRF are due to what?

A

Uremic Toxin buildup in CSF - fluid overload occurs

177
Q

What sort of multi system effects occur from alterations in the neurologic system from CRF

A

Cognition and consciousness changes from memory issues to confusion, disorientation, coma, convulsion, and even death

decreased concentration and attention span

decreased libido and impotence

muscle cramping (from hypocalcemia)

abnormal EEGs

ANS issues

behavior changes

peripheral neuropathy

178
Q

What is an abnormal EEG indicative of in CRF

A

metabolic encephalopathy

179
Q

What occurs from ANS dysfunction in CRF

A

orthostatic hypotension because baroreceptors in the carotid and aorta are not responding due to the urea

180
Q

What behavior changes occur in CRF

A

personality changes

increased irritability

labile emotions

agitated depression

delusions

psychosis

181
Q

What are the manifestations of peripheral neuropathy in CRF

A

gait changes

burning feet

restless legs

foot drop

cranial nerve issues with vision, hearing and smell

intestinal tract issues

urinary bladder issues (UTI or no urine made)

182
Q

How do the peripheral neuropathy issues occur in CRF

A

they are symmetric and begin distally and work their way inward

183
Q

Osteodystrophy

A

the disruption of normal calcium and phosphorus feedback loop leading to abnormal bone growth and major long term complications beginning early in CRF like bone pain, deformities, and fractures

184
Q

In healthy adults, if serum calcium drops what happens

A

Parathyroid gland releases PTH –> this stimulates kidney production of activated Vitamin D which is needed for calcium absorption in the small intestine–> this leads to increased calcium reabsorption and phosphorus excretion in the urine as well as stimulation of calcium release from bone

185
Q

What is the Result of PTH as a compensatory mechanisms

A

Return to normal calcium, phosphorus, and PTH levels

186
Q

Why does PTH not work in CRF

A

In CRF kidneys cannot produce activated vitamin D OR excrete phosphorus

So phosphorus levels will rise and serum calcium will fall leading to PTH production –> the parathyroid gland will maintain calcium for a little bit by drawing calcium and phosphorus from bone –> eventually as kidney disease progresses the compensation mechanism goes haywire and leads to secondary hyperparathyroidism

187
Q

What happens after the secondary hyperparathyroidism begins in CRF

A

Parathyroid gland continues to make PTH and becomes hypertrophic –> number and sensitivity of Vitamin D decrease and parathyroid gland becomes less responsive to calcium and vitamin D –> over time the bones respond less and less to PTH so more is needed to maintain typical rate of bone turnover —> as a result body’s ability to replace old bone with healthy new bone is compromised

188
Q

Consequences of Parathyroid activity in CRF

A

abnormally high levels of PTH

hypocalcemia (or hypercalcemia if there is chronic hyperparathyroidism)

hyperphosphatemia

renal osteodystrophy

189
Q

People with secondary hyperparathyroidism can end up with..;.

A
  1. Osteitis Fibrosa

2.Osteomalacia

  1. Both!
190
Q

Osteitis Fibrosa

A

high turnover bone disease

an osteodystrophy

191
Q

Osteomalacia

A

low turnover bone disease

an osteodystrophy

192
Q

Both osteitis fibrosa and osteomalacia lead to what

A

weakened bones and increases the risk of fractures

193
Q

Osteitis Fibrosa occurs from

A

hyperphosphatemia

hypocalcemia

low levels of activated vitamin D

secondary hyperparathyroidism

194
Q

Osteomalacia occurs from

A

Aluminum intoxication

This is because aluminum blocks CA uptake in bone causing demineralization

195
Q

What manifestations occur in the body from Osteitis Fibrosa and Osteomalacia

A

muscle weakness

bone pain and tenderness

spontaneous fracture (even from something like a cough from croup)

196
Q

Without ____ calcium cannot be absorbed

A

vitamin D

197
Q

How does Uremia lead to no calcium absorption

A

it inhibits vitamin D production and synthesis

198
Q

How does Uremia ultimately effect the musculoskeletal system in CRF

A
  1. Decreased Absorption of Ca from intestines
  2. Decreased serum Ca and high phosphate levels d/t catabolism
  3. Parathyroid glands release PTH
  4. Ca is pulled from bone causing demineralization (osteomalacia)
  5. Ca and PO4 precipitate in cardiovascular tissue, liver, and joint tissue
  6. Pathological fractures and bone changes occur followed by “Red Eyes”
199
Q

What causes CRF Red Eyes

A

Calcium Phosphate deposits in the eye

200
Q

Treatments for the Musculoskeletal problems in CRF

A
  1. Activated Vitamin D therapy
  2. Parathyroidectomy
  3. Calcium Acetate or Carbonate - Not aluminum hydroxide gels
201
Q

Calcitrol and Dihydrotachysterol (DHT)

A

activated forms of Vitamin D

202
Q

Why may a parathyroidectomy be done in CRG

A

if hyperplasia occurs and starts functioning autonomously regardless of Serum Ca and Phosphate levels it may need removal to prevent osteodystrophy

203
Q

Why do we no longer give aluminum hydroxide gels to CRF patients

A

it can lead to Osteomalacia

204
Q

What do we give now rather than aluminum hydroxide gels to treat musculoskeletal problems in CRF

A

calcium acetate or carbonate

ex: phoslo or TUMS

205
Q

TUMS c an be used for what purposes?

A
  1. Dyspepsia
  2. Allowing calcium absorption to occur
206
Q

How does the skin function change with CRF

A
  1. Calcium Phosphate concentration products greater than 60-70 occur
  2. Salt Wasting
  3. Anemia
  4. Hyperparathyroidism
  5. High concentration of metabolic end products end up in body fluids
207
Q

What are the manifestations of skin alterations in CRF

A

extracellular calcifications (CaPhos Deposits)

dry skin and mucous membranes (Salt wasting)

pale and sallow complexion (anemia)

pruritis (urea)

uremic frost and odor of urine on skin and breath - embarrassing for people

208
Q

What sort of things can you see on the skin in a person with CRF

A

itching, crawling skin from deposits of urea and phosphates – > scratching causes excoriations that heal poorly

pallor from anemia and also a yellow brown or gray color from retained urinary pigments

bruises from capillary fragility and clotting defects

dry scaly skin from decreased oil gland activity and loss of subcu tissue

uremic frost made of urate cryustals

brittle thin spoon shaped nails from anemia

dry scaly hair that falls out easily

petechiae

209
Q

Calciphylaxis

A

Usually fatal syndrome of vascular calcification, thrombosis and skin necrosis

occurs in ESRD

210
Q

What is manifested in calciphylaxis

A

ischemic skin lesions with areas of necrosis appearing as violaceous lesions or completely black lesions

extensive on the body

happens because of calcium deposits in the blood vessels stopping blood flow

211
Q

What is needed to diagnose calciphylaxis

A

skin biopsy to confirm

212
Q

Changes in GU system function from CRF

A

impaired general health

decreased testosterone and estrogen

213
Q

Manifestations of Altered GU function in CRF

A

impotence

loss of libido

amenorrhea

214
Q

What kind of diet is needed for CRF

A

low quantity high quality proteins to reduce end products of protein metabolism the kidneys cannot excrete

low sodium

low potassium

fluid restriction to maintain fluid balance (can lead to always feelings thirsty)

215
Q

What amount and what kind of proteins should be given to a CRF patient

A

0.5-1 g/kg of body weight daily of low quantity high quality complete proteins

these proteins have all the essential acids to increase anabolism (RBC, plasma, muscle proteins) and decrease catabolism (uremic waste)

216
Q

Why is the diet for CRF low sodium and potassium

A

low sodium to prevent further fluid overload

low potassium since the kidney cannot rid K (salt substitutes for K must be avoided too)

217
Q

How is fluid balance monitored in CRF?

A

through weight gain between dialysis treatments

218
Q

What sort of medications are given in conservative therapy of CRF

A

Diuretics

Antihypertensives

Alkalizing Agents

Cation Exchange Resin

Anti emetics, Anti diarrheals, laxatives

Dietary supplements

synthetic erythropoietin

anticonvulsants

supplements

antipruitics

other vitamin supplements

219
Q

Why are CRF pts given diuretics

A

to treat fluid overload and HTN

Thiazides and aldosterone antagonists are given

220
Q

Why must one be careful giving aldosterone antagonists like Aldactone to CRF patients?

A

its a diuretic but it is potassium sparing

221
Q

Why are CRF pts given antihypertensives

A

to control BP and edema

ace inhibitors and beta blockers

222
Q

What is better for CRF patients, ace inhibitors or beta blockers

A

beta blocks because ace inhibitors can slow aldosterone making it hard to rid of K

223
Q

Why are CRF pts given alkalizing agents

A

to treat metabolic acidosis

its sodium bicarbonate or sodium citrate

224
Q

Why are CRF pts given Cation exchange resins

A

Na for K resins to treat hyperkalemia

insulin to use the GIK mechanism to get K into cells

Kayexalate to excrete K

calcium gluconate to depress myocardial irritability by raising thresholds

sodium bicarb

225
Q

What level of K is a medical emergency

A

higher than 7 mEq/L

226
Q

Why are CRF pts given anti emetics, anti diarrheas’, and laxatives

A

to relieve vomiting, nausea, constipation or gastric irritation

227
Q

What to be aware of when giving anti emetics, anti diarrheals or laxatives to CRF patients

A

cannot give something like Aluminum or Milk of Magnesia because you need to give them something WITHOUT MAGNESIUM since they cannot excrete Mg either

228
Q

Why are CRF pts given dietary supplements like iron and folic acid

A

to treat anemia

oral or parenteral iron because low protein diets are low in iron
folic acid is water soluble and is loss in dialysis so it should be replaced

229
Q

Why are CRF pts given synthetic erythropoietin

A

Epogen

in order to get the reticulocyte count up

230
Q

Why are CRF pts given anticonvulsants

A

to treat neurologic symptoms

231
Q

Why are CRF pts given supplements like vitamin D (calcitriol) and calcium acetate/carbonate

A

to treat osteodystrophy

vitamin D will be an active form to bind calcium for absorption

calcium acetate or carbonate will lower serum K levels

232
Q

Why are CRF pts given antipruritics?

A

to relieve itching

ex: Benadryl

233
Q

What are some other vitamin supplements given to CRF patients

A

vitamin C (water soluble)

multivitamins with B complex and vitamin D

234
Q

1 in 10,000 with ESRD need what?

A

Dialysis treatment or a Kidney transplant

235
Q

What are the top 2 reasons for ESRD

A
  1. Diabetic Glomerulosclerosis (Nephropathy)
  2. Hypertensive Nephroangiosclerosis

both kill the kidney

236
Q

What are some other reasons for ESRD

A

chronic glomerulonephritis

chronic pyelonephritis (reflux)

Polycystic kidney disease (PKD)

237
Q

What racial group has a higher risk for ESRD and why

A

African americans d/t higher risk for HTN

238
Q

Nephrosclerosis accounts for how many cases in African Americans compared to Caucasians?

A

1/3 of AA CRF cases

only 8% of cauc. cases

N361: Pathophysiology II (20 decks)

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