Brainscape's Knowledge GenomeTM

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


See full index

Pathophysiology > Renal > Flashcards

Renal Flashcards

1
Q

Juxtamedullary nephrons vs Cortical Neohrons

A

Juxtamedullary nephron reach into the medulla with a long loop of Henly. They have think loops of Henly into the inner stripe allowing these nephrons to be predisposed to damage from low blood flow. 10% of our total nephrons Cortical nephrons do not extend into the inner zone. Less likely to be damaged. 90% of our total nephrons

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

What is the equation for calculating GFR

A

(Urine Cr (mg/ml) * Volume Urine (ml/min)) / Plasma Cr (mg/ml) GFR= (((140-age) * lean weight (kg)) / (Plasma Cr * 72)) * 0.85

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  1. Loop diuretics block what channel? 2. Thiazide diuretics block what channel?
A
  1. Na+-K+-2Cl- pump 2. Block Na+ reabsorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Geriatric Considerations with the Kidneys

A
  1. Loss of Nephrons 2. Diminished Renal Blood Flow 3. Decreased GFR 4. Decreased ability to conserve salt and water
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What can cause an increase in BUN with no renal damage?

A

Dietary protein intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  1. Azotemia 2. Uremia
A
  1. elevation in BUN and Cr levels related to decrease GFR 2. Elevation of urea in the blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
  1. Nephrolithiasis 2. Glumerulonephritis
A
  1. Renal Stones 2. inflammation of the glumeruli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where is Kidney pain usually found?

A

Felt at the Costovertebral angle posteriorly and can follow the T10-L2 dermatomes around to anterior. *Back and Flank Pain

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

Polycystic Kidney Disease — Genetics and What is going on in the kidney

A

-Development of cysts inside the kidney that can lead to obstruction of urine flow and renal failure - Can be autosomal dominant or recessive -

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Polycystic Kidney Disease -Clinical Manifestations -Treatment

A

Clinical Manifestations –Pain –HTN –Concomitant cystic liver involvement Treatment –Supportive – Dialysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Renal Cell Carcinoma -Manifestations -Predisposig Factors -Treatment

A

Manifestations –Tumor of the kidney (can be primary or secondary) —-Primary large, secondary seedlike –Can lead to Kidney Failure Predisposing Factors –Familial pattern –Smoking, Obesity, HTN Treatment –Nephrectomy

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

Normal Protective mechanisms of the kidney against infections (6)

A
  1. Acidic pH 2. Presence of Urea in Urine 3. Men: Bacteriostatic prostate secretions 4. Women: Glands in distal uretha secrete mucous 5. Micturition: Washed out pathogens 6. Unidirectional Urine Flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pyelonephritis 2 causes

A

–Ascending infection from lower Urinary Tract (common) –Bacteremia

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

Chronic Pyelonephritis –Manifestations –Treatment

A

Usually caused by reflux or obstructive process leading to urine stasis Manifestations –abd/flank pain, fever, malaise Treatment –Correct underlying process –Antimicrobial therapy

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

Complete Urine Obstruction can result in?

A
  1. Hydronephrosis 2. Decreased GFR 3. Ischemic Kidney Damage (b/c of increased intralumenal pressures) 4. Acute Tubular Necrosis 5. Chronic Kidney Disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Nephrolithiasis (Renal Stones) –What are they made from? Why do they form? Manifestations?

A
  • Crystal Aggregates of organic and inorganic materials Calcium Crystals (most common)
  • Can be made of uric acid, phosphate, or Oxalate (struvite, cystine)
  • Manifestations
    • Intense renal colic pain with abrupt onset
    • N/V
    • Hematuria
17
Q

Nephrolithiasis –Treatment and prevention

A

Treatment – >2L fluids/day to pass stone –Lithotripsy can be used –Urethral Stenting –Pain medications Prevention –Stones tend to reoccur —Prevent with high fluid intake —–Also Dietary calcium prevents stone formation by binding oxalate and preventing absorption

18
Q

Nephrotic Syndrome –What is it characterized by? Disease processes causing? Symptoms

A

-Glomerular permeability to proteins -Urinary loss of >3.5 g protein/day Disease Processes Causing -SLE, DM, Minimal Change Disease Symptom -Edema -Hyperlipidemia (liver making many proteins) -Hypercoagulability (liver making proteins)

19
Q

Nephrotic Syndrome Treatment

A

-Diurectics -Lipid Lowering Agents -Antihypertensives -Immunosuppression

20
Q

Minimal Change Disease –What? Who? Symptoms? Treatment?

A

What? Deceased production of anions by the podocytes. Initiated by an allergic or immune condition Who? Children Symptoms? Sudden onset edema, nephrotic levels of protein loss, hypoalbuminemia Treatment? Corticosteroids

21
Q

Acute Glomerulonephritis –What? Manifestations? Treatment?

A

–Inflammation in the kidney from possible infection, resulting in degradation of the basement membrane. –GFR may fall due to contraction of the mesangial cells. Manifestations –Proteinuria, Oliguria, Azotemia, HTN, Edema Treatment –Steroids –ABX –Plasmapheresis –Supportive measures including HTN support

22
Q

Berger Disease

What?

Manifestations?

Prognosis?

A
  • IgA Nephropathy
  • Most common diagnosed
    • Common in adults
  • Follows upper resp or GI infection
  • Complex deposition and degradation causes injury to mesangial cells
  • Manifestations –No Proteinuria, Edema, or HTN
    • hematuria presents in 1-2 days in the form of casts
  • Prognosis –Variable, can progress to ESRD
23
Q

Chronic Glomerulonephritis What? Who? Treatment?

A

Progressive degradation of the kidney with collagen formation, ultimately leading to ESRD. Defined with slowly declining renal function Who? Multiple Sclerosis, ALS Treatment? Supportive with ultimately a Kidney transplant needed

24
Q

Normal BUN:Cr ratio

A

10:1 or 20:1

25
Q

ARF BUN:Cr rations for Prerenal, Intrarenal, Postrenal and why these numbers are seen?

A

Prerenal– >20:1– both BUN and Cr have decreased filtration but urea has more time to be reabsorbed Intrarenal– <10:1– Tubules are failing, less urea reabsorbed Post Renal– 10-20:1– Both Urea and Cr affected equally

26
Q

Possible Causes of Acute Renal Failure (ARF) (7)

A

Hypotension – Overuse of Diuretics, Burns, Vomiting, Diarrhea, Edema 2. Renal Artery Obstruction 3. Drugs– Ace Inhibitors, NSAIDS

27
Q

How to NSAIDs damage the kidney?

A

Block prostaglandins, prostaglandins provide vasodilation in the efferent arteriole, thereby causing vasoconstriction in the efferent arteriole and increased pressure within the glomerulus.

28
Q

Acute Tubular Necrosis (ATN)

A

Can be caused by decreased O2 to the outer medulla. –Cells die and slough off the tubule wall occluding tube. –Casts of dead cells are formed –increased intratubular and glomerular pressure –Increased tubular leaking into the medulla. –Reduced GFR and Oliguria *Good prognosis if no other comorbidities

29
Q

Three Phases of ATN

A
  • Prodromal Phase (immediate)
    • Injury has occured
    • Incerased BUN and Cr
  • Oliguric Phase (1-8 weeks)
    • Oliguria/anuria
    • Volume Overload
    • Hyperkalemia
    • Metabolic Acidosis
  • Postoliguric Phase (2 days-1 year)
    • Fluid Volume Deficeit
    • Labs begin to normalize
30
Q

Chronic Kidney Disease

A

Decreased Kidney function for 3 or more months –Kidneys can compensate till 75-80% of glomeruli are damaged *Know the stages in the assessment lecture

31
Q

Common Causes of CKD

A
  1. DM 2. HTN 3. Recurrent Polynephritis 4. Glomerulonephritis 5. Over 65 yoa 6. Polycystic Kidney Disease 7. Exposure to Toxins 8. Ethnicity
32
Q

Clinical Considerations of CKD

A
  • HTN–Use ACE inhibitors
  • Control Glucoses
  • Manage ATN
  • Allow metabolic Acidosis
    • acidosis <7.30 treat with NaHCO3
    • acidosis 7.30-7.35 requires no treatment
  • Uremic Syndrome- retention of wastes
  • Electrolyte imbalances
  • Anemia- Lack of EPO —-EPO production correlates with GFR
33
Q

Extra-Renal manifestations of CKD

A
  1. HTN— r/t renin release 2. Pulm Edema– secondary to fluid retention 3. Depressed Immune function 4. N/V and Anorexia 5. Anemia 6. Neuropathies
34
Q

How does Dialysis function?

A

Blood is removed from the body and run thru a tube within a solute bath. Solutes move via osmosis and thereby filter the blood. The blood is then returned to the patient. **You want a Dialysis soln that has electrolyte values slightly lower than that of the blood, BUT has a higher osmotic pressure to pull fluid from the blood.

35
Q

Prostate Problems

A

BPH- Usually starts in central zone of the prostate and squeezes the urethra causing occusion Prostate Cancer– Usually starts in the peripheral zone and does not form any symptoms until late stage often times. ** See Coexisting for TURP procedures

Pathophysiology (26 decks)

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