Rr-Symptoms-Ckd

Front 1

Stage 1 CKD

Back 1

GFR > 90 with renal damage as evident by proteinuria

Front 2

Stage 2 CKD

Back 2

GFR 60-89

Front 3

Stage 3 CKD

Back 3

GFR 30-59 (A and B)

Front 4

Stage 4 CKD

Back 4

GFR 15-29

Front 5

Stage 5 CKD

Back 5

GFR < 15

Front 6

Pt was diagnosed with type 2 Diabetes
Mellitus 10 years ago. At that point he was on oral
hypoglycemic drugs. Now he presents with main
complaint of leg swelling and polyuria. On Exam he
is 5’11”, 278 lbs, temp 37, RR 17, pulse 98, BP
167/102. Lungs are clear on auscultation. He has
3+ LE edema bilateral and symmetrical.

Most likely cause of LE edema?

Back 6

Kidney disease complications of DM

Although DVT is plausible, it is unlikely because the edema is bilateral.

Front 7

Diabetic Nephropathy

Back 7

Among the leading cause of nephrotic syndrome which have a constellation of features: Proteinuria (>3/5g/24hr), hypoalbuinemia, hyperlipidemia and edema. The edema is caused by volume retention (salt retaining nephrons) and low oncotic pressure caused by hypoalbuminemia.

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Front 10

On further interview he said that he is get tired and
wants to lay down during the day especially after he
takes his meds in the morning. His current medications
are metformin, clonidine, glyburide, and Lasix. What
are the possible cause(s) of his fatigue?
A. Hypoglycemia
B. Obstructive sleep
apnea
C. Hypotension
D. TIAs

Back 10

Hypoglycemia
Hypotension

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Back 11

Front 12

Central alpha 2 agonists

Back 12

Clonidine
Guanabenz
alpha-methyldopa

Stimulate alpha2-adrenergic receptors in the brain
- this reduces sympathetic outflow from the brains vasomotor center
- increases vagal tone

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Back 13

Front 14

Central alpha 2 agonists: adverse effects

Back 14

- sodium and water retention
- abrupt discontinuation may cause rebound htn
- depression
- orthostatic htn
- dizziness

clonidine can result in anticholinergic side effects

methyldopa can cause hepatitis, hemolytic anemia (rare)

Front 15

With this patient what labs are necessary?

Back 15

- Blood chemistry (BMP, HbA1C)
- Urine albumin/creatinine ratio
- Lipids profile

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Front 18

53 year old female with family history of
autosomal dominant polycystic kidney disease
(ADPKD). She just moved from another state 10
month ago. She was told 14 years ago that she
has polycystic kidney disease but nothing to be
worried about yet. She was busy but now has to
see someone because she noticed she has blood
in the urine and she has right flank pain. Vitals:
Temp 37°C, RR 16, Pulse 72, BP 176/105. Pt is
only taking ibuprofen for headache.

What is the most likely cause of her
symptoms ?

Back 18

Kidney Stones
Ruptured Renal Cyst

Front 19

Renal Complications of Autosomal Dominant Polycystic Kidney Disease

Back 19

Infection
Kidney Stones
Hematuria
Renal cell carcinoma is suspected when hematuria is recurrent or perisistent

Front 20

Diagnosis for PKD

Back 20

1. Imaging technology of cysts in kidneys and other organs
2. Family medical history (genetic testing)

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Front 22

Ascending Limb Loop of Henle

Back 22

- Sodium and chloride reabsorbed (20-30%): active chloride reabsorbed

- Impermeable to water: no water reabsorption

- Can compensate for increased sodium delivery from proximal tubule by increasing reabsorption

- Diuretic action on cortical and medullary segments differ in response

Front 23

Characteristics of Thiazide and Thiazide-like Diruectics

Back 23

Orally active
Intermediate efficacy (8-10% of
filtered sodium load excreted)
Moderate onset of activity (60 min)
Long duration of action

Front 24

Mechanism of action of thiazide diuretics

Back 24

Filtered and secreted by the OAT
Inhibits Na-Cl symporter
Acts on cortical segment of distal tubule
Increases the excretion of sodium,
potassium, chloride and water
Urine is hypertonic – unable to dilute

Increases potassium secretion
Enhances urate reabsorption

Front 25

Disadvantages of thiazide diuretics

Back 25

Hypokalemia
Alkalosis
Hyperuricemia
Hyperglycemia
Decrease in GFR with thiazies

Front 26

Uses of thiazide diuretics

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Edema due to CHF
Hypertension
Hyeprcalciuria/Ca salt - renal caliculi

Front 27

Loop Diuretics

Back 27

Furosemide, Bumetanide, Ethacrynic Acid

Front 28

Characteristics of Loop Diuretics

Back 28

Orally and IV active
High efficacy (20-30% of filtered sodium load excreted)
Rapid in onset (20-30min)
Short duration of action

Front 29

Mechanism of Loop Diuretics

Back 29

Filtered and secreted by OAT
Inhibits Na-K-2Cl symporter
Acts on the cortical and medullary segments of the ascending limb of the loop of Henle
Increase the excretion of sodium, potassium, chloride, and water

Front 30

Actions of Loop Diuretics?

Back 30

Increases renal blood flow and GFR
Enhances calcium excretion
Large urine volume

Front 31

Disadvantages and side effects of Loop Diuretics

Back 31

Hypokalemia
Alkalosis
Hypovolemia
Hyperuricemia (urate reabsorption - PT)
Hyperglycemia - furosemise
Otoxicity

Front 32

Uses of Loop Diuretics

Back 32

Edema of cardiac, hepatic or renal origin
Acute pulmonary edema
HTN

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Front 34

Patient has the following:
Blood chemistry come back showing
– eGFR 18
– Ca 7.1
– Hemoglobin 8.5
– PO4 7.8
– PTH 328

What should you give them?

Back 34

Erythropoietin
Calcitriol
Phosphate binders

Front 35

Tolvaptan

Back 35

Vasopressin receptor 2 antagonism
Was designed to treat hyponatremia
cAMP carry out the signal of V2 receptor
In PKD cAMP also stimulates cystogensis and increase the size of cysts
Drug gas been shown to reduce cyst growth

Front 36

Main complications of Tolvaptan

Back 36

One of the main complications is volume loss

Front 37

What is the likely chemical changes seen on BMP on first blood draw in ER with Tolvaptan

Back 37

- Creatine
- Sodium
- BUN

Front 38

Creatinine goes up when GFR goes down.
Why?

Back 38

Decreased kidney function leads to a decreased ability in creatinine clearance

Front 39

Pt decided to withdraw from the clinical trial. eGFR is
stable.
Two month later she calls your office and said she has
the worst headache of her life. What should the
advice be?

Back 39

Call 911 or go to nearest ER

Front 40

Extra-renal complications of ADPKD?

Back 40

Intracranial aneurysm: 5-7% of adults with ADPKD may
have brain aneurysm and up to 12-15% if another family
member had an intracranial aneurysm. (5x higher than
general population)
• Liver cysts: >85 percent of patients will have liver cysts
by age 30.
• Heart valve disease: 25% of patients with ADPKD.
Usually require no treatment but can become severe
enough to require valve replacement.
• Abdominal wall hernias: 45 % of patients with ADPKD.

Front 41

A 45-year-old morbidly obese Caucasian woman
comes to your office for the first time to
establish care. She has not seen a doctor in
years and complains only of wanting to lose
weight. The patient takes no medications and
has no significant past medical history. Her
parents are both living and healthy. Her blood
pressure is 145/88mm Hg and BMI is 40.5. The
remainder of her exam is normal. You order a
fasting lipid profile, basic serum chemistry
panel, urinalysis, and electrocardiogram.

Regarding her obesity and risk for kidney
disease, what information will you give
her?

Back 41

Obesity may cause proteinuria

Front 42

Obesity-associated glomerulosclerosis

Back 42

form of hyperfiltration nephropathy, in which hemodynamic changes associated with obesity lead to progressive renal scarring, decline in glomerular
filtration rate, and proteinuria. It is a known entity, whose incidence is rising with the epidemic of obesity in the United States

Front 43

Obesity leads to hypertension via

Back 43

increased peripheral resistance and an increase in cardiac output, increased sympathetic tone and increased salt sensitivity(Kasper).

Front 44

The patient is a 52-year-old male with polycystic kidney disease. Despite a strict diet, his symptoms of fatigue, pruritus, and headache recently have gotten worse, and he has episodes of hematuria and urinary tract infections almost every month. He has gained several pounds during the last week despite a low appetite. On examination, patient is edematous, has uremic fetor, sallow colored skin with "uremic
frost," and slightly icteric sclera. His blood pressure is
190/120. Laboratory shows normochromic normocytic
anemia, metabolic acidosis, and the imbalance of potassium, sodium, and chlorides, with increased levels of calcium, phosphate, and magnesium, and with reduced bicarbonate. Blood urea nitrogen (BUN) and creatinine levels are elevated. Urinalysis reveals the presence of proteinuria, hematuria, bacteriuria, and leucocyturia. His glomerular filtration rate
(GFR) is 14 mL/min/1.73 square meters. This patient should start dialysis.

What should also be administered?

Back 44

Erthropoietin

Front 45

Best medication for lowering the BP of a morbidly obese woman with diabetes?

Back 45

ACE-I

Front 46

A 45-year-old white female comes for her annual
checkup. She has been seen regularly over the last
10 years. She has had Adult Onset Diabetes for the
past 10 years. Her weight is 205 pounds at a height
of 5 feet 1 inch. She is unsuccessful in losing weight.
Her blood pressure is 170/95, temperature is 97.6 F,
and heart rate is 82. High blood pressure and
diabetes are the most common cause of end-stage
renal disease in the United States. In a normal
kidney when the blood pressure reaches >150
mmHg the body's ability to auto regulate
glomerular capillary pressure will start to fail. In
talking with the client, you explain that her blood
pressure should be optimally below 127/75.

What is causing his polyuria?

Back 46

Nephrogenic diabetes insipidus

lithium impairs the distal water reabsorption, mediated by vasopressin (ADH), leading to the production of large quantities of dilute urine. Unfortunately, lithium use, even for as short a
period as 1 year, can lead to irreversible damage of the tubules (via down-regulation and production of receptors and channels responsible for water reabsorption).

Front 47

Treatments for lithium-induced nephrogenic diabetes
insipidus include

Back 47

amiloride, a distal-tubule acting diuretic which competes with lithium for access to ion channels and thus prevents the lithium-induced polyuria,
and B) hydrochlorothiazide with a low-salt diet, in order to effectively decrease the quantity of urine produced. Depakote can be substituted for lithium, but as mentioned above, lithium may cause irreversible tubular damage

Front 48

Central Diabetes Insipidus

Back 48

amiloride, a distal-tubule acting diuretic which competes with lithium for access to ion channels and thus prevents the lithium-induced polyuria,
and B) hydrochlorothiazide with a low-salt diet, in order to effectively decrease the quantity of urine produced. Depakote can be substituted for lithium, but as mentioned above, lithium may cause irreversible tubular damage

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Front 50

A 59-year-old African American man with a past medical history of hypertension, benign prostatic hypertrophy, type II diabetes mellitus for the past 15 years, and chronic back pain presents to the hospital with gross hematuria. The patient states that he noticed blood in his urine last night. The patient also reports mild, intermittent flank pain. The patient states that his diabetes and blood pressure are well controlled with medications, and that he has managed his chronic back pain with 2 aspirin per
day for the past 4 years. Vital signs are Temp- 98.6°F, BP- 124/82 mm/Hg, pulse- 88/min, and RR- 14/min. Blood work is notable for HbA1C of 6.5%. A pyelogram reveals a ring sign. His current fasting glucose is 140mmol/L.

Most likely cause of hematuria?

Back 50

Analgesic Nephropathy

Front 51

Analgesic Nephropathy

Back 51

The fact that this patient has been taking aspirin regularly for the past 4 years puts him at great risk for analgesic nephropathy. These patients occasionally present with gross hematuria.

Front 52

A 60-year-old man presents to the emergency room with severe, tearing pain radiating to the upper back. Over a period of hours, the pain moves to the mid back and then involves both flanks. Hematuria develops shortly thereafter. What renal complication is likely associated with the patient's symptoms?

Back 52

Bilateral renal infarction

Front 53

Bilateral Renal Infarction can result in?

Back 53

Dissecting aortic aneurysm that occluded the renal arteries, causing bilateral renal infarction with flank pain and hematuria. This is a very dangerous complication of dissecting aortic aneurysm

Front 54

Acute glomerulonephritis

Back 54

characterized by hematuria, red cell casts, and often proteinuria and edema. This syndrome typically develops over days, not hours, and would not be expected to result from dissecting aortic aneurysm.

Front 55

Polycystic kidney disease

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Lifelong condition characterized by bilateral polycystic changes in the kidneys. It is associated with hypertension and eventual renal failure.

Front 56

Polynephritis

Back 56

infection of the kidney that can develop as a complication of bacterial endocarditis, or as a consequence of vesicoureteral reflux, but would not be expected to result from aortic dissection.

Front 57

Sickle Cell Crisis

Back 57

can cause papillary necrosis of the kidneys with hematuria, but there is no indication that the patient has sickle cell anemia.