Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Kidney Disease > Acute Kidney Disease > Flashcards

Acute Kidney Disease Flashcards

1
Q

Where are the kidneys located?
How large are they?

A
  • Behind the peritoneum
  • T12 to L3
  • A little bigger than the fist (4-5 inches long)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What makes up the renal hilum?

A

Renal vein
Renal nerve
Renal artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the main function of the kidneys?

A

Filter blood / excrete toxins –> remove waste and toxic substances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the other functions of the kidneys?

A

Metabolize compounds (drugs, toxins, xenobiotics)

Secrete hormones (Endocrine functions)

Maintain pH (acid-base) and electrolyte balance –> Produce Bicarbonate –> Neutralize H+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does kidney disease present itself?

A

Kidney disease is usually silent until advanced

No pain receptors in the kidney

Pain is usually not present (except for kidney stones)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the functional component of the kidney?

A
  • Nephron
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the vasculature of the kidneys?

A
  • Afferent Arteriole
  • Glomerulus
  • Efferent Arteriole
  • Peritubular capillaries line the tubes of the nephrone into the medulla
  • Interlobular vein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where are nephrons locate din the kidney?

A

The nephrons are located in the cortex and medulla of the kidney. The cortex contains the renal corpuscle, distal convoluted tubule and proximal convoluted tubule. Whereas, the medulla contains the loop of Henle and collecting ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the flow through a nephron

A
  • Bowmans Capsule
  • Proximal Tubule
  • Descending Limb of the loop of Henle
  • Asceding loop of Henle
  • Distal Tubule
  • Collecting Duct
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the average filtration rate of the kidneys?

A
  • 100-120 mL/min
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What size of molecules can be filtered by the kidney?

A

Small molecules (typically dissolved < 70 kDa) are filtered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Can larger than 70 kDa be filtered?
Example of immune related damage.

A

Yes –> Possible if glomerular damage

50—60 KDA  sometimes can filter in, sometimes not completly

A protein may get stuck on the surface of the glomerulus  If this happens, this part becomes the target for the immune system  Caus einflmmation and dmage to the glomerulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the role of the proximal tubule? What molecules?

A

Substantial reabsorption (back into blood) of filtered material

60-70% of filtered Na+, almost all K+, almost all glucose

Water reabsorbed passively along osmotic gradients of Na+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does reabsorption in the kidneys work? (process from kidneys to blood)

A

Tubule –> Interstitial Space –> Capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Filtration rate of the loop of Henle

A

30 mL/min of filtrate delivered to loops of Henle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where is the loop of Henle located?

A

Loop passes into the middle (medulla) of kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the role of the loop of Henle?

A

Substantial Na+ and water reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

The Ascending limb is responsible….

A
  • Reabsorption of Na+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

The descending limb is responsible for….

A

reabsorption of water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Filtration rate of the distal tubule and collecting duct

A

5-10 mL/min delivered to collecting ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

In the distal tubule and collecting duct, what hormone stimulates water reabsorption?

A
  • Vasopressin (antidiuretic hormone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Vasopressins role in the distal and collecting duct

A
  • Stimulates water reabsorption alone (i.e., without Na+)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

The distal tubule and collecting duct is the target for what hormone? What is its role?

A

aldosterone – causing Na+ reabsorption and K+ excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Aldosterone acts on….. to…..

A

Distal tubule/collecting duct is also the target for aldosterone – causing Na+ reabsorption and K+ excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where is pH regulation in the nephron occuring?

A
  • Distal tubule and collecting duct
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How does the distal tubule and collecting duct regulate pH?

A

Respond towards acidosis by increasing H+ secretion and HCO3- generation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How many mL of filtrate enters the ureters and the bladder?

A

1-2 ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What occurs in the proximal tubule (mainly)? Why is this important for drugs?

A

Throughout the tubules, channels actively secrete (and reabsorb) compounds into (and out of) the urine
Happens in the proximal tubule section
Many drugs and toxins are excreted this way

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the channels responsible for NaCl reabsorption?

A

NCC: Thiazide Sensitive NaCl cotransporter

ENaC: Amiloride-sensitive epithelial sodium channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Thiazide Drug Type? MOA?

A

Thiazide is a diuretic

  • Inhibits NCC channel, preventing Na+ and Cl- reabsorption, therefore stimulating water reaborption, lower blood pressure
  • K+ rebsorbed and excreted in urine –> Hypokalemia potential
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Amiloride Drug Type? MOA?

A
  • potassium-sparing diuretic which can decrease potassium execretion at distal tubule
  • inhibits ENaC channel, inhibits Na+ reaborption, water reabsorbed, lower blood pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the most commonly used marker of kidney function?

A
  • Creatinine level in the blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the normal range of creatinine in the blood?

A
  • 0.9-1.3 mg/dL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Why is creatinie produced?

A

Produced daily by muscles as part of their normal metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Why is creatinine used as a marker of kidney function?

A

Easily filtered, so level does not typically rise UNLESS glomerular filtration rate is reduced
Serum level of creatinine can be used to estimate GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What happens to creatine when GFR decreases?

A

Less creatinine is excreted
Production by muscle continues
Creatinine level in the blood (i.e., serum creatinine) rises

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What can happen to someones creatinie level if they have a low muscle mass?

A

People with low muscle mass will generate less creatinine
Thus, even if GFR is decreased, the serum creatinine may appear within normal limits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the Crockroft-Gault equation?

Why is it an important concept?

Female?

A

CrCl =((140 −age) x Ideal Body Weight (kg))/(0.814 x Serum Creatinine (μM)) (x 0.85 if female)

converts serum creatinine level to an estimated GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How can one estimate ideal body weight?

A

IBW typically used (unless underweight)
IBW for a 5’0” tall person ( 50 kg for men and 45 kg for women)
Add 2.3 kg for every 1” taller than 5’0”
Male 5’10”: IBW = 73kg
Female 5’10”: IBW = 68kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What does the MDRD stand for? What is it used for? How is it calculated?

A

DRD: Modification of Diet in Renal Disease
We can also use MDRD equation to estimate GFR
GFR (mL/min/1.73 m2) =175× (Scr)-1.154× (Age)-0.203× (0.742 if female) × (1.212 if African American)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Why is it important for pharmacists to know a patients GFR?

A

Pharmacists need to be aware of patients’ kidney functions at all times
Many drugs require dosage reduction when renal function is less than optimal
If dosage adjustment is not performed, regular doses will be excreted more slowly, leading to accumulation of drug in the body and risk for adverse drug reactions (ADR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the major factors influencing whether a drug is excreted renally?

A
  1. Water Solubility
  2. Protein Binding
  3. Tubular Secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How does water solubility affect renal drug excretion?

A

Drugs that are highly soluble can exist freely in the bloodstream (in solution)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How does protein binding affect renal drug excretion?

A

Drugs that are highly bound to plasma proteins are less likely to be filtered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How does tubular secretion affect drug renal excretion? WHich drugs?

A

Some drugs are concentrated in the urine by active secretion rather than (or in addition to) filtration (metformin, furosemide, digoxin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Estimated GFR can often be used for….

A
  • Staging chronic kidney disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Staging of Chronic Kidney Disease

A

Study the CHART

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is proteinuria? What is it useful for?

A

Protein in the urine – another sign of kidney damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Proteinuria is a common marker of…

A

dysfunction in patients with CKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Proteinuria is a good marker of dysfunction because

A

Can be elevated without reduced GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is an early marker of kidney disease?

A

Low level of albumin in the urine serves as an early marker of kidney disease (specifically, glomerular dysfunction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is albuminuria?
What are the types and there levels?

A

Albuminuria is a more sensitive marker than total protein
Microalbuminuria = 30-300 mg/day
Macroalbuminuria (overt albuminuria) > 300 mg /day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the albumin/creatinine ratio?

A

a simple spot urine test that accurately predicts microalbuminuria (more convenient than collecting urine for 24 hrs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the albuminuria stages?

A

Look at colourful chart (KNOW IT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Kidney Proteinuria can be measured by…..

A

Urinalysis
X-ray
MRI
CT
Ultrasounds
Biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is AKI? Definition

A

Rapid deterioration of renal function within a few hours or a few days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

AKI is diagnosed when….

A

Typically diagnosed if either of the following occur:
Rise in SCr by more than 25 μM within 48 hrs OR
Decrease in urine output to < 0.5 mL/kg/hr for at least 6 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

AKI results in….. (4 things)

A

Rapidly rising BUN/urea (i.e., azotemia) and SCr
BUN: blood urea nitrogen
Diminished urine volume common (but not necessary)
Cause a build-up of waste products in blood
Affect other organs such as the brain, heart, and lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

AKI is often confusing because….

A

Highly complex and often overlapping
Many mechanisms of AKI are possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Are drugs a major cause of AKI?

A

Most individual drugs confer a small chance of AKI (<1%)

Considering the widespread use of drugs in Canada, drug-induced AKI is a relatively common reason for hospital admission
Present in 5-7% of hospital admissions and 1/3 of admissions to the intensive care unit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Who is AKI most common in?

A

Patients with chronic kidney disease (CKD) are more susceptible to AKI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the symptoms of AKI?

A

Too little urine leaving the body
Swelling in legs, ankles, and around the eyes –> Build up of waste and water
Fatigue or tiredness
Shortness of breath
Confusion
Nausea
Seizures or coma in severe cases
Chest pain or pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are the causes of AKI? What are they?

A

renal azotemia
Reduced glomerular pressure impairing function of tubules

Intrinsic renal parenchymal disease
Direct damage to glomerulus, tubules, or renal vessels

Postrenal obstruction
Obstruction of urine outflow

(Dance Party People At O2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is pre-renal azotemia? Can it be reversed?

A

nitrogen increase in blood

Defined as rise urea (and SCr) from reduced glomerular pressure WITHOUT signs of tubular damage

Completely reversible if addressed before damage occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Pre-renal azotemia presentation initially and later?

A

Urine is maximally concentrated, however, once damage is present the ability to concentrate urine declines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Pre-renal azotemia commonly arises from….

A

Reduced cardiac output (CO) –> less blood
Hypovolemia –> less blood; not the heart
Medications (NSAIDs and RAAS inhibitors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Reduced cardiac output results in…..

A

Decreased GFR, Increase SCr, Increased BUN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Afferent vasoconstriction or reduced blood flow results in

A

Decreased GFR, Increased SCr, increased BUN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What can cause severe volume depletion?

A

major bleed, GI fluid losses (diarrhea), burns (loss through skin), etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Severe volume depletion results in….

A
  • Decreased GFR, increased SCr, Increased BUN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Examples of Reno-vascular disease

A

renal artery stenosis (by atherosclerosis OR other vascular wall conditions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Reno-vascular disease results in…..

A

Dcreased GFR, increased SCr, Increased BUN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

NSAIDS can cause AKI through what 2 mechanism s…

A

Reduction of renal blood flow OR
Direct injury (interstitial nephritis)

Even low-dose aspirin has the potential to impact renal function (albeit at a low risk)

74
Q

NSAIDS can result in a….

A
  • Decreased GFR, increased SCr, and increased BUN
75
Q

Intra-renal damage can occur in the nephron at….

A

Glomerulus / glomerular structures
Tubules or interstitial space (between tubules)
Vascular conditions

76
Q

Glomerular injury cause, main population. Is it reversible?

A

Chronic injury to the glomerulus is often a result of longstanding glomerular pressure along with other factors
Chronic glomerular injury is MOST commonly-observed in patients with diabetes and HTN***
Glomerular injury can be irreversible

77
Q

Immune-related glomerular injury mechanism

A

Glomerular capillary wall is susceptible to immune-mediated injury
Antigens and antibodies tend to get “caught” in the structure (probably due to high blood flow and high pressure)
Immune system may react to parts of the glomerular apparatus directly (autoimmunity)

78
Q

How can drugs cause tubular injury?

A

Kidneys are programmed to concentrate solutes within tubules, resulting in high concentrations
Presence of numerous channels results in high exposure of certain drugs WITHIN renal cells
If toxins are present, they can cause damage to tubular, interstitial, and endothelial cells

79
Q

Acute Tubular Necrosis Mechanism

A

Nephrotoxic drugs leading to endoplasmic reticulum stress leading to protein misfolding or ischemia/repurfusion leading to oxidative stress in mitochondria can cause the creation of reactive oxygen species (free radicals, peroxidases) leading to oxidative cell damage in acute tubular necrosis leading to cell apoptosis or necrosis

80
Q

Direct Toxicity –> Cisplatin Induced AKI Mechanism

A

Accumulates in proximal tubular cells
Causes direct toxicity
Pre-hydration (to dilute the drug in the tubules) has decreased the risk of AKI
The cancer clinic has a specific protocol that must be followed for all patients receiving cisplatin-based chemotherapy regimens

81
Q

Rhabdomyolysis

A

A syndrome resulting from the release of myoglobin (Mw = 16.7 kDa) into the bloodstream

Myoglobin can precipitate in renal tubules – halting tubular flow, leading to tubular cell necrosis

82
Q

What is myoglobin?

A

Myoglobin is an oxygen-binding protein found in muscle cells (related to Hemoglobin)

83
Q

What does rhabdomyolysis present itself?

A

muscle pain/weakness, malaise, and dark urine (if myoglobin concentration is very high)

84
Q

What are some causes of rhabdomyolysis?

A

Traumatic / crush injuries
Non-traumatic muscle compression, prolonged immobility
Exertional (e.g., +++exertion in untrained people, hyperthermia)
Drugs / toxins (e.g., infections, electrolyte disorders, drugs (STATINS)

85
Q

Interstitial Nephritis occurs where

A

Occurs when spaces between tubules become inflamed
Inflammation generally spreads to tubules but spares glomeruli

86
Q

Interstitial nephritis is often called….
Mechanism and Incidence?

A

Often called “hypersensitivity” reactions (penicillins, NSAIDs, sulfonamide antibiotics) because no injury appears to take place before the reaction
Exact mechanism not clear
Incidence is very low

87
Q

Ischemia-associated AKI - How much oxygen does a normal healthy kidney recieve?

A

Healthy kidneys receive 20-25% of cardiac output and account for 10% of resting O2 consumption

88
Q

What is ischemia-associated AKI? What is the region sensitive to?

A

Inner region of the kidney (medulla) operates under relative hypoxic conditions even in healthy people
This region is especially sensitive to:
Persistent pre-renal azotemia
Small vessel inflammation (vasculitis)
Atherosclerosis
Other occlusions to blood flow

89
Q

Atherosclerotic Vascular Disease Mechanism

A

Likely an important cause of CKD as a result of chronic renal ischemia

Reduce blood flow in large vessels

Renal damage from vascular disease may be very slow

Likely overshadowed by ischemic events in other organs (brain, heart)

People with CKD are at very high risk for A-CV events
Likely because of the link with atherosclerosis

90
Q

How does Intrinsic AKI Causes present itself in comparison to extrinsic causes?

A

AKI due to intrinsic (or intra-renal) causes will have very similar clinical presentations

91
Q

Intrinsic AKI Diagnosis

A

Usually, the only way to confirm the diagnosis is from renal biopsy

92
Q

Tx of Intrinsic AKI

A

Treatment options are extremely limited other than discontinuing the offending agent

93
Q

Intrinsic AKI Necrosis Reversibility

A

It is important to remember that tubular necrosis can be reversible in the setting of AKI (i.e., AKI does not always result in CKD)

94
Q

What are the two causes of kidney stones?

Are they painful?

A

Usually due to “idiopathic hypercalciuria” (>75% of stones contain calcium)

Uric acid stones result from hyperuricosuria (especially in patients with history of gout)

Can be very painful

95
Q

Kidney Stone Formation and cause of pain

A

Result from alterations in the solubility of various substances in the urine
Stone formation in the kidney is painless, thus, renal damage and hematuria can occur in the absence of pain
Pain is due to the distention of the ureter, renal pelvis or renal capsule

96
Q

Kidney Stone Risk Factors

A

Dehydration (high fluid intake recommended > 2L/day)

Protein intake (protein can increase blood and urine acidity leading to Ca or uric acid stones in vulnerable people)

High Na intake (increases Ca excretion)

97
Q

Is calcium intake an indicator of kidney stone formation?

A

Calcium intake actually may NOT play a big role

98
Q

Kidney Stone Symptoms and Tx

A

Pain, hematuria, and even ureteral obstruction (if it occurs) are usually self-limiting
For smaller stones, passage usually requires only fluids, bed rest, and analgesia

99
Q

Kidney Stone Complications Prescence and Examples

A

Complications can occur but are rare

Damage from complete blockage of urine and back-up of toxins and pressure

Infection or abscess

Repeated stones may cause accumulated damage

100
Q

How is AKI classified?

A

RIFLE

Risk of renal dysfunction
Injury to the kidney
Failure of kidney function
Loss of kidney function
End-stage renal disease (ESRD)

101
Q

RIFLE Criteria

A
  • Memorize Chart
102
Q

AKIN Classification

A

Modification of RIFLE

Memorize Chart

103
Q

How is AKI diagnosed?

A

Urine output test
Urinalysis
Blood test
Imaging test – X-ray, CT, MRI and ultrasounds
Kidney biopsy (renal needle biopsy and open kidney biopsy)

104
Q

What are some complications of AKI?

A

Pulmonary edema (fluid buildup in lungs) → respiratory failure
Anemia
Chest pain (pericarditis → inflammation of pericardium)
Muscle weakness (due to unbalance of fluids and electrolytes)
Hyperkalemia
Metabolic acidosis
Permanent kidney damage (occasionally)
Death

9Every animal can mate, how about donkey d***)

105
Q

How does pulmonary edema occur in AKI?

A

Pulmonary epithelial Na,K-ATPase, ENaC and aquaporin 5 are downregulated in AKI

Downregulation of Na,K-ATPase and ENaC
Decrease the transport of fluids out of alveoli
Downregulation of aquaporin 5
May reduce pulmonary secretion

Pulmonary inflammation

106
Q

Kidney Injury and Kidney Failure Impact on the Lungs

A

Injury –> More inflammation, some non-hydrostatic edema
Failure –> Less inflammation, more non-hydrostatic edema

107
Q

Hyperkalemia Definition

A

Higher potassium level in the blood

108
Q

Hyperkalemia in AKI is due to injuries where in the nephron….

A

injuries to distal convoluted tubule and collecting duct

109
Q

A common complication for AKI is….

A

Hyperkalemia

110
Q

Aldosterone’s target is….and it is responsible for…..

A

Distal tubule/collecting duct is the target for aldosterone – causing Na+ reabsorption and K+ excretion

111
Q

Metabolic Acidossis is caused by……

A

Loss of bicarbonate by the kidneys
- Decrease in pH as body still produces H+

112
Q

Symptoms of metabolic acidosis are….

A

Can cause nausea, vomiting, shortness of breath, etc.

113
Q

What are some risk factors for AKI?

A

Hospitalization: ICU
Aging
Cardiovascular diseases, such as heart failure
Hypertension
Diabetes
Kidney diseases
Liver diseases
Certain types of cancer and cancer treatment

114
Q

Can AKI be easily prevented?

A

Very difficult to prevent AKI

115
Q

The risk of AKI can be reduced by….

A

Living a healthy lifestyle
Managing kidney and other chronic conditions
Paying attention to drug labels, especially for the OTCs

116
Q

Cancer chemotherapy associated AKI can be prevented by…..

A

Pre-hydration and allopurinol a few days before chemotherapy

117
Q

Exposure to nephrotoxic medications AKI can be prevented by….

A

Avoid nephrotoxic medications if possible, measure and follow drug levels, and adjust doses and intervals

118
Q

Exposure to radiographic contrast agents can be prevented by…..

A

Avoid intravenous contrast media, and use iso- or low-osmolar contrast agents at lowest volume

119
Q

Hemodynamic instability associated AKI can be prevented by…..

A

Optimal fluid resuscitation

120
Q

Liver failure AKI can be prevented by…..

A

Avoid hypotension and GI bleeding

121
Q

Rhabdomysis associated AKI can be prevented by…..

A

Maintain adequate hydration

122
Q

Undergoing surgery. To prevent AKI we would….

A

Adequate volume of resuscitation, and prevention of hypotension

123
Q

How can AKI be treated?

A

Patients should be hospitalized
Management of AKI is primarily supportive
Requiring collaboration among primary physicians, nephrologists, hospitalists and other specialists in the care team

Key to treatment: maintaining adequate renal perfusion and avoiding hypovolemia

Treat underlying causes
Treat complications until kidneys recover

124
Q

In AKI, we treat the ……

A
  • Underlying causes and complications until the kidneys recover
125
Q

What are the 3 molecules we want to maintain in AKI?

A

Water
Potassium
Calcium

126
Q

In regards to balance of body fluid, how can excess and less body fluid be treated?

A

Less body fluid → IV fluids
Extra body fluid → diuretics

127
Q

Potassium level complications can be treated by…..

A

High blood potassium → arrhythmias

Prescribe calcium, glucose (moves K+ into cells, reduce level in blood) or sodium polystyrene sulfonate (Non-digestable, Na+ replaced by K+)

128
Q

How can Ca2+ modulate K+ serum levels?

A

Calcium does not reduce K+ LEVEL, BUT REDUCES THE CHANCE OF GETTING AN ARRYHTHYMIA by moving serum K+ into cells

129
Q

Polystyrene Sulfonate MOA and Use

A

Non-digestable, Na+ replaced by K+
- Used for tx of hyperkalmeia

130
Q

In AKI, blood Ca2+ levels may be…. therefore we treat this by….

A

Low blood calcium → IV infusion of calcium gluconate

131
Q

In AKI, what may accumulate in the body as a complication? How is this treated?

A
  • Remove toxins via dialysis
132
Q

How can kidney failure be treated?

A

Treatment of kidney failure

133
Q

How does kidney dialysis work?

A

Perform the normal function of kidney
Remove toxins, wastes and extra fluid from the blood

134
Q

What are the two types of kidney dialysis?

A

Hemodialysis
Peritoneal dialysis

135
Q

The most common type of dialysis is…..

A

Hemodialysis

136
Q

Hemodialysis uses a….. to…. This is returned to…

A

Use a hemodialyzer

Blood is removed from the body and filtered by the hemodialyzer

Filtered blood is returned to the body

137
Q

_____ Acess is needed for hemodialysis. This can be done through…..

A

Vascular Acess

Arteriovenous (AV) fistula (preferred). (1)
AV graft. (2)
Vascular access catheter. (3)

138
Q

AV Fistula is……

A

Small surgery to connect artery and vein together

Does not go through the capillaries

139
Q

What are the benefits and downfalls of an AV fistula?

A

less likely to get an infection and clot

Permenant –> Connection needs to mature (3-4 months wait time after surgery)

Not good for people with weak veins

140
Q

An AV graft is a……

A

a tube to connect the tubes

141
Q

What are the benefits and downfalls of an AV graft?

A

Recovery time –> 2-3 weeks
Inside the body –> Quick;

Higher chance of infection and blood clots

Good for people with smallr veins

Overtime, the tube needs to be replaced

142
Q

A Vascular Acess Cathether dialysis is a…..

A
  • Catheter inserted into the vein of the arm, and strung down to the kidney
  • Easy insertion, easy access, faster dialysis, we do not need to wait, dialysis can be conducted immediately
143
Q

What are the benefits and downfalls of vascular access catheter?

A

Easy to get blood clot and infection
Can cause damage to the vein if done multiple times
Can leave the catheter in there if need dialysis next day
Higher chance of infection and blood clots –> If do several times, can get damage to the vein

144
Q

Peritoneal dialysis main job

A

Remove wastes and toxins from the blood when kidneys are no longer functional

145
Q

Peritoneal Dialysis Mechanism of Function

A

Dialysis fluid (water with salt and additives) is flowed from a bag into the peritoneal cavity via a catheter
The lining of peritoneum acts as a filter
The dialysis solution absorbs wastes and extra fluid
After several hours, the solution, along with the wastes, is drained out into an empty bag

146
Q

What are the two types of peritoneal dialysis?

A

Continuous ambulatory peritoneal dialysis (CAPD)

Automated peritoneal dialysis

147
Q

How are diuretics classified?

A

Classified based on their site of action in the nephron and on their mechanism

148
Q

Diuretics (in general) MOA

A

Increase renal excretion of water and salt from the body

149
Q

What is the evidence for diuretics use in AKI?

A

No clear evidence showing diuretics help in treatment of AKI
Diuretics may even increase in-hospital mortality and nonrecovery of renal function

150
Q

Thiazide Diuretics Include

A

Chlorothiazide
Hydrochlorothiazide
Chlorthalidone
Indapamide
Metozalone

151
Q

Loop Diuretic Example

A

Furosemide
Torsemide
Bumetanide
Ethacrynic Acid

152
Q

Potassium-Sparing Diuretic Examples

A

ENAC Blockers:
- Amiloride
- Triamterene

Aldosterone Receptor Antagonists:
- Spironolactone
- Eplerenone

153
Q

Osmotic Diuretics Examples

A
  • Mannitol (main one)
  • Glycerin
  • Isosorbide
  • Urea
154
Q

Diuretics Usages Include

A

Hypertension
Heart failure
Hepatic cirrhosis
Renal insufficiency
Edema

155
Q

Thiazide diuretics site of action

A

Distal convoluted tubules

156
Q

Thiazide diuretics MOA

A

Block Thiazide-sensitive NaCl cotransporter

Build up of Na+ in there, osmotic pressure, water goes into the lumen, a lot of water and Na+ there

Since sodium load is so high, body keeps pumping potassium out trying to equalize –> Lose K+

Signal –> When Na+ level is high, wants to reabsorp Na+ and excrete K+
Body excretes K+, but Na+ reabsorption is blocked

157
Q

Thiazide diuretic primary use

A

Hypertension

158
Q

What are the common adverse effects of thiazide diuretics?

A

Hypovolemia → orthostatic hypotension, dizziness
Hyperglycemia → caution in diabetics
Tinnitus
Photosensitivity
GI disturbance

159
Q

Loop Diuretics Site of Action

A

ascending limb of loop of Henle

160
Q

Loop Diuretics MOA

A

Block luminal Na/K/2Cl co-transporter (NKCC2)

161
Q

Which is more potent: Thiazide or Loop?

A

Loop Diuretics

162
Q

The primary use of loop diuretics…..

A

Acute pulmonary edema, congestive heart failure, etc.

163
Q

Adverse effects of loop diuretics include…..

A

Electrolyte losses – sodium, chloride, potassium
Hypotension
Ototoxicity –> Fluid changes in inner ear
Hyperuricemia –> High uric acid level, protein metabolism
Hyperglycemia
Increased serum triglycerides
Increased LCL-cholesterol
Muscle cramps

164
Q

Where is the potassium-sparing diuretics site of action?

A

Collecting Duct

165
Q

What are the two types of Potassium sparing diuretics?

A

ENaC Blockers: amiloride-sensitive epithelial sodium channels

Aldosterone receptor antagonists

166
Q

The aldosterone receptor are responsible for…..

A

Na+ reabsorption and K+ excretion

167
Q

ENAC Blocker Examples

A

Amiloride
Triamterene

168
Q

Aldosterone Receptor Antagonist Examples

A

Spironolactone

Eplereone

169
Q

Potassium-sparing diuretics main use is for people….

A

at risk of low potassium level

170
Q

Do potassium sparing diuretics reduce blood pressure?

A

NO

171
Q

What is the least potent diuretic?

a) Thiazide
b) Loop
c) Potassium Sparing
d) Osmotic

A

C

172
Q

What are some common adverse effects of potassium-sparing diuretics? (all)

A

Hyperkalemia → cardiac arrythmias; watch dietary potassium intake

Muscle cramps

173
Q

Spironolactone Adverse Effects

A

Diarhhea
Cramping
Gastritis
Abnormal Liver Function
Androgenic Effects
Gynecomastia

174
Q

Amiloride Specific Adverse Effects

A

Abdominal Pain
Loss of Appetite
Rash

175
Q

Most common osmotic diuretic

A

Mannitol

176
Q

Where does mannitol work?

A

Proximal Tubule
Descending Limb
Collecting Duct

177
Q

Mannitol Filtration

A
  • freely filtered at the glomerulus
178
Q

Osmotic MOA

A

Limited reabsorption in renal tubules
Produces osmotic gradient and retains water in the tubules

179
Q

Adverese Effects of Osmotics

A

Electrolyte Depletion
Worsen CHF or Pulmonary Edema initially
Headache
Nauseau/Vomitting
Blurred Vision
Diziness

180
Q

Why can osmotic diuretics worsen CHF and pulmonary edema? When?

A
  • At initiation of tx
  • Due to increase in ECF volume

Kidney Disease (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions