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)
2
Q
What makes up the renal hilum?
A
Renal vein
Renal nerve
Renal artery
3
Q
What is the main function of the kidneys?
A
Filter blood / excrete toxins –> remove waste and toxic substances
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+
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)
6
Q
What is the functional component of the kidney?
A
- Nephron
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
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
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
10
Q
What is the average filtration rate of the kidneys?
A
- 100-120 mL/min
11
Q
What size of molecules can be filtered by the kidney?
A
Small molecules (typically dissolved < 70 kDa) are filtered
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
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+
14
Q
How does reabsorption in the kidneys work? (process from kidneys to blood)
A
Tubule –> Interstitial Space –> Capillaries
15
Q
Filtration rate of the loop of Henle
A
30 mL/min of filtrate delivered to loops of Henle
16
Q
Where is the loop of Henle located?
A
Loop passes into the middle (medulla) of kidney
17
Q
What is the role of the loop of Henle?
A
Substantial Na+ and water reabsorption
18
Q
The Ascending limb is responsible….
A
- Reabsorption of Na+
19
Q
The descending limb is responsible for….
A
reabsorption of water
20
Q
Filtration rate of the distal tubule and collecting duct
A
5-10 mL/min delivered to collecting ducts
21
Q
In the distal tubule and collecting duct, what hormone stimulates water reabsorption?
A
- Vasopressin (antidiuretic hormone)
22
Q
Vasopressins role in the distal and collecting duct
A
- Stimulates water reabsorption alone (i.e., without Na+)
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
24
Q
Aldosterone acts on….. to…..
A
Distal tubule/collecting duct is also the target for aldosterone – causing Na+ reabsorption and K+ excretion
25
Where is pH regulation in the nephron occuring?
- Distal tubule and collecting duct
26
How does the distal tubule and collecting duct regulate pH?
Respond towards acidosis by increasing H+ secretion and HCO3- generation
27
How many mL of filtrate enters the ureters and the bladder?
1-2 ml/min
28
What occurs in the proximal tubule (mainly)? Why is this important for drugs?
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
29
What are the channels responsible for NaCl reabsorption?
NCC: Thiazide Sensitive NaCl cotransporter
ENaC: Amiloride-sensitive epithelial sodium channels
30
Thiazide Drug Type? MOA?
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
31
Amiloride Drug Type? MOA?
- potassium-sparing diuretic which can decrease potassium execretion at distal tubule
- inhibits ENaC channel, inhibits Na+ reaborption, water reabsorbed, lower blood pressure
32
What is the most commonly used marker of kidney function?
- Creatinine level in the blood
33
What is the normal range of creatinine in the blood?
- 0.9-1.3 mg/dL
34
Why is creatinie produced?
Produced daily by muscles as part of their normal metabolism
35
Why is creatinine used as a marker of kidney function?
Easily filtered, so level does not typically rise UNLESS glomerular filtration rate is reduced
Serum level of creatinine can be used to estimate GFR
36
What happens to creatine when GFR decreases?
Less creatinine is excreted
Production by muscle continues
Creatinine level in the blood (i.e., serum creatinine) rises
37
What can happen to someones creatinie level if they have a low muscle mass?
People with low muscle mass will generate less creatinine
Thus, even if GFR is decreased, the serum creatinine may appear within normal limits
38
What is the Crockroft-Gault equation?
Why is it an important concept?
Female?
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
39
How can one estimate ideal body weight?
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
40
What does the MDRD stand for? What is it used for? How is it calculated?
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)
41
Why is it important for pharmacists to know a patients GFR?
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)
42
What are the major factors influencing whether a drug is excreted renally?
1. Water Solubility
2. Protein Binding
3. Tubular Secretion
43
How does water solubility affect renal drug excretion?
Drugs that are highly soluble can exist freely in the bloodstream (in solution)
44
How does protein binding affect renal drug excretion?
Drugs that are highly bound to plasma proteins are less likely to be filtered
45
How does tubular secretion affect drug renal excretion? WHich drugs?
Some drugs are concentrated in the urine by active secretion rather than (or in addition to) filtration (metformin, furosemide, digoxin)
46
Estimated GFR can often be used for....
- Staging chronic kidney disease
47
Staging of Chronic Kidney Disease
Study the CHART
48
What is proteinuria? What is it useful for?
Protein in the urine – another sign of kidney damage
49
Proteinuria is a common marker of...
dysfunction in patients with CKD
50
Proteinuria is a good marker of dysfunction because
Can be elevated without reduced GFR
51
What is an early marker of kidney disease?
Low level of albumin in the urine serves as an early marker of kidney disease (specifically, glomerular dysfunction)
52
What is albuminuria?
What are the types and there levels?
Albuminuria is a more sensitive marker than total protein
Microalbuminuria = 30-300 mg/day
Macroalbuminuria (overt albuminuria) > 300 mg /day
53
What is the albumin/creatinine ratio?
a simple spot urine test that accurately predicts microalbuminuria (more convenient than collecting urine for 24 hrs)
54
What are the albuminuria stages?
Look at colourful chart (KNOW IT)
55
Kidney Proteinuria can be measured by.....
Urinalysis
X-ray
MRI
CT
Ultrasounds
Biopsy
56
What is AKI? Definition
Rapid deterioration of renal function within a few hours or a few days
57
AKI is diagnosed when....
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
58
AKI results in..... (4 things)
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
59
AKI is often confusing because....
Highly complex and often overlapping
Many mechanisms of AKI are possible
60
Are drugs a major cause of AKI?
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
61
Who is AKI most common in?
Patients with chronic kidney disease (CKD) are more susceptible to AKI
62
What are the symptoms of AKI?
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
63
What are the causes of AKI? What are they?
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)
64
What is pre-renal azotemia? Can it be reversed?
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
65
Pre-renal azotemia presentation initially and later?
Urine is maximally concentrated, however, once damage is present the ability to concentrate urine declines
66
Pre-renal azotemia commonly arises from....
Reduced cardiac output (CO) --> less blood
Hypovolemia --> less blood; not the heart
Medications (NSAIDs and RAAS inhibitors)
67
Reduced cardiac output results in.....
Decreased GFR, Increase SCr, Increased BUN
68
Afferent vasoconstriction or reduced blood flow results in
Decreased GFR, Increased SCr, increased BUN
69
What can cause severe volume depletion?
major bleed, GI fluid losses (diarrhea), burns (loss through skin), etc.
70
Severe volume depletion results in....
- Decreased GFR, increased SCr, Increased BUN
71
Examples of Reno-vascular disease
renal artery stenosis (by atherosclerosis OR other vascular wall conditions)
72
Reno-vascular disease results in.....
Dcreased GFR, increased SCr, Increased BUN
73
NSAIDS can cause AKI through what 2 mechanism s...
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
NSAIDS can result in a....
- Decreased GFR, increased SCr, and increased BUN
75
Intra-renal damage can occur in the nephron at....
Glomerulus / glomerular structures
Tubules or interstitial space (between tubules)
Vascular conditions
76
Glomerular injury cause, main population. Is it reversible?
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
Immune-related glomerular injury mechanism
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
How can drugs cause tubular injury?
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
Acute Tubular Necrosis Mechanism
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
Direct Toxicity --> Cisplatin Induced AKI Mechanism
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
Rhabdomyolysis
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
What is myoglobin?
Myoglobin is an oxygen-binding protein found in muscle cells (related to Hemoglobin)
83
What does rhabdomyolysis present itself?
muscle pain/weakness, malaise, and dark urine (if myoglobin concentration is very high)
84
What are some causes of rhabdomyolysis?
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
Interstitial Nephritis occurs where
Occurs when spaces between tubules become inflamed
Inflammation generally spreads to tubules but spares glomeruli
86
Interstitial nephritis is often called....
Mechanism and Incidence?
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
Ischemia-associated AKI - How much oxygen does a normal healthy kidney recieve?
Healthy kidneys receive 20-25% of cardiac output and account for 10% of resting O2 consumption
88
What is ischemia-associated AKI? What is the region sensitive to?
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
Atherosclerotic Vascular Disease Mechanism
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
How does Intrinsic AKI Causes present itself in comparison to extrinsic causes?
AKI due to intrinsic (or intra-renal) causes will have very similar clinical presentations
91
Intrinsic AKI Diagnosis
Usually, the only way to confirm the diagnosis is from renal biopsy
92
Tx of Intrinsic AKI
Treatment options are extremely limited other than discontinuing the offending agent
93
Intrinsic AKI Necrosis Reversibility
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
What are the two causes of kidney stones?
Are they painful?
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
Kidney Stone Formation and cause of pain
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
Kidney Stone Risk Factors
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
Is calcium intake an indicator of kidney stone formation?
Calcium intake actually may NOT play a big role
98
Kidney Stone Symptoms and Tx
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
Kidney Stone Complications Prescence and Examples
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
How is AKI classified?
RIFLE
Risk of renal dysfunction
Injury to the kidney
Failure of kidney function
Loss of kidney function
End-stage renal disease (ESRD)
101
RIFLE Criteria
- Memorize Chart
102
AKIN Classification
Modification of RIFLE
Memorize Chart
103
How is AKI diagnosed?
Urine output test
Urinalysis
Blood test
Imaging test – X-ray, CT, MRI and ultrasounds
Kidney biopsy (renal needle biopsy and open kidney biopsy)
104
What are some complications of AKI?
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
How does pulmonary edema occur in AKI?
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
Kidney Injury and Kidney Failure Impact on the Lungs
Injury --> More inflammation, some non-hydrostatic edema
Failure --> Less inflammation, more non-hydrostatic edema
107
Hyperkalemia Definition
Higher potassium level in the blood
108
Hyperkalemia in AKI is due to injuries where in the nephron....
injuries to distal convoluted tubule and collecting duct
109
A common complication for AKI is....
Hyperkalemia
110
Aldosterone's target is....and it is responsible for.....
Distal tubule/collecting duct is the target for aldosterone -- causing Na+ reabsorption and K+ excretion
111
Metabolic Acidossis is caused by......
Loss of bicarbonate by the kidneys
- Decrease in pH as body still produces H+
112
Symptoms of metabolic acidosis are....
Can cause nausea, vomiting, shortness of breath, etc.
113
What are some risk factors for AKI?
Hospitalization: ICU
Aging
Cardiovascular diseases, such as heart failure
Hypertension
Diabetes
Kidney diseases
Liver diseases
Certain types of cancer and cancer treatment
114
Can AKI be easily prevented?
Very difficult to prevent AKI
115
The risk of AKI can be reduced by....
Living a healthy lifestyle
Managing kidney and other chronic conditions
Paying attention to drug labels, especially for the OTCs
116
Cancer chemotherapy associated AKI can be prevented by.....
Pre-hydration and allopurinol a few days before chemotherapy
117
Exposure to nephrotoxic medications AKI can be prevented by....
Avoid nephrotoxic medications if possible, measure and follow drug levels, and adjust doses and intervals
118
Exposure to radiographic contrast agents can be prevented by.....
Avoid intravenous contrast media, and use iso- or low-osmolar contrast agents at lowest volume
119
Hemodynamic instability associated AKI can be prevented by.....
Optimal fluid resuscitation
120
Liver failure AKI can be prevented by.....
Avoid hypotension and GI bleeding
121
Rhabdomysis associated AKI can be prevented by.....
Maintain adequate hydration
122
Undergoing surgery. To prevent AKI we would....
Adequate volume of resuscitation, and prevention of hypotension
123
How can AKI be treated?
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
In AKI, we treat the ......
- Underlying causes and complications until the kidneys recover
125
What are the 3 molecules we want to maintain in AKI?
Water
Potassium
Calcium
126
In regards to balance of body fluid, how can excess and less body fluid be treated?
Less body fluid → IV fluids
Extra body fluid → diuretics
127
Potassium level complications can be treated by.....
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
How can Ca2+ modulate K+ serum levels?
Calcium does not reduce K+ LEVEL, BUT REDUCES THE CHANCE OF GETTING AN ARRYHTHYMIA by moving serum K+ into cells
129
Polystyrene Sulfonate MOA and Use
Non-digestable, Na+ replaced by K+
- Used for tx of hyperkalmeia
130
In AKI, blood Ca2+ levels may be.... therefore we treat this by....
Low blood calcium → IV infusion of calcium gluconate
131
In AKI, what may accumulate in the body as a complication? How is this treated?
- Remove toxins via dialysis
132
How can kidney failure be treated?
Treatment of kidney failure
133
How does kidney dialysis work?
Perform the normal function of kidney
Remove toxins, wastes and extra fluid from the blood
134
What are the two types of kidney dialysis?
Hemodialysis
Peritoneal dialysis
135
The most common type of dialysis is.....
Hemodialysis
136
Hemodialysis uses a..... to.... This is returned to...
Use a hemodialyzer
Blood is removed from the body and filtered by the hemodialyzer
Filtered blood is returned to the body
137
_____ Acess is needed for hemodialysis. This can be done through.....
Vascular Acess
Arteriovenous (AV) fistula (preferred). (1)
AV graft. (2)
Vascular access catheter. (3)
138
AV Fistula is......
Small surgery to connect artery and vein together
Does not go through the capillaries
139
What are the benefits and downfalls of an AV fistula?
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
An AV graft is a......
a tube to connect the tubes
141
What are the benefits and downfalls of an AV graft?
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
A Vascular Acess Cathether dialysis is 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
What are the benefits and downfalls of vascular access catheter?
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
Peritoneal dialysis main job
Remove wastes and toxins from the blood when kidneys are no longer functional
145
Peritoneal Dialysis Mechanism of Function
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
What are the two types of peritoneal dialysis?
Continuous ambulatory peritoneal dialysis (CAPD)
Automated peritoneal dialysis
147
How are diuretics classified?
Classified based on their site of action in the nephron and on their mechanism
148
Diuretics (in general) MOA
Increase renal excretion of water and salt from the body
149
What is the evidence for diuretics use in AKI?
No clear evidence showing diuretics help in treatment of AKI
Diuretics may even increase in-hospital mortality and nonrecovery of renal function
150
Thiazide Diuretics Include
Chlorothiazide
Hydrochlorothiazide
Chlorthalidone
Indapamide
Metozalone
151
Loop Diuretic Example
Furosemide
Torsemide
Bumetanide
Ethacrynic Acid
152
Potassium-Sparing Diuretic Examples
ENAC Blockers:
- Amiloride
- Triamterene
Aldosterone Receptor Antagonists:
- Spironolactone
- Eplerenone
153
Osmotic Diuretics Examples
- Mannitol (main one)
- Glycerin
- Isosorbide
- Urea
154
Diuretics Usages Include
Hypertension
Heart failure
Hepatic cirrhosis
Renal insufficiency
Edema
155
Thiazide diuretics site of action
Distal convoluted tubules
156
Thiazide diuretics MOA
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
Thiazide diuretic primary use
Hypertension
158
What are the common adverse effects of thiazide diuretics?
Hypovolemia → orthostatic hypotension, dizziness
Hyperglycemia → caution in diabetics
Tinnitus
Photosensitivity
GI disturbance
159
Loop Diuretics Site of Action
ascending limb of loop of Henle
160
Loop Diuretics MOA
Block luminal Na/K/2Cl co-transporter (NKCC2)
161
Which is more potent: Thiazide or Loop?
Loop Diuretics
162
The primary use of loop diuretics.....
Acute pulmonary edema, congestive heart failure, etc.
163
Adverse effects of loop diuretics include.....
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
Where is the potassium-sparing diuretics site of action?
Collecting Duct
165
What are the two types of Potassium sparing diuretics?
ENaC Blockers: amiloride-sensitive epithelial sodium channels
Aldosterone receptor antagonists
166
The aldosterone receptor are responsible for.....
Na+ reabsorption and K+ excretion
167
ENAC Blocker Examples
Amiloride
Triamterene
168
Aldosterone Receptor Antagonist Examples
Spironolactone
Eplereone
169
Potassium-sparing diuretics main use is for people....
at risk of low potassium level
170
Do potassium sparing diuretics reduce blood pressure?
NO
171
What is the least potent diuretic?
a) Thiazide
b) Loop
c) Potassium Sparing
d) Osmotic
C
172
What are some common adverse effects of potassium-sparing diuretics? (all)
Hyperkalemia → cardiac arrythmias; watch dietary potassium intake
Muscle cramps
173
Spironolactone Adverse Effects
Diarhhea
Cramping
Gastritis
Abnormal Liver Function
Androgenic Effects
Gynecomastia
174
Amiloride Specific Adverse Effects
Abdominal Pain
Loss of Appetite
Rash
175
Most common osmotic diuretic
Mannitol
176
Where does mannitol work?
Proximal Tubule
Descending Limb
Collecting Duct
177
Mannitol Filtration
- freely filtered at the glomerulus
178
Osmotic MOA
Limited reabsorption in renal tubules
Produces osmotic gradient and retains water in the tubules
179
Adverese Effects of Osmotics
Electrolyte Depletion
Worsen CHF or Pulmonary Edema initially
Headache
Nauseau/Vomitting
Blurred Vision
Diziness
180
Why can osmotic diuretics worsen CHF and pulmonary edema? When?
- At initiation of tx
- Due to increase in ECF volume
