Renal Flashcards

1
Q

Describe Macro Renal Terms-

Hilus
Renal Pelvis

A

Hilus- Where all nerves and vessels enter kidney, Notch of kidney bean.

Renal Pelvis- The funnel like dilated end of the ureter that
collects urinefrom end of nephrons

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2
Q

Describe Micro Renal terms-

Nephron

Glomerulus

A

Nephron- functional unit of kidney includes vascular component connected to circulatory and tubular component connected circ and elimination functions of kidney. Bowman’s capsule and onward

Glomerulus- Capillary Bed (filtration) has afferent and efferent arterioles. Filtrate into capsule and then more reabsorption and ecretion happens in peritubular capillary beds

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3
Q

Describe Lower UTI

Incidence, infectious agent, from where, progression?

A
  • Common
  • Variety of Bacteria (usually E. Coli)
  • Urine is sterile, but normal flora in external genitalia
  • More common in women
  • Ascending infection
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4
Q

Describe our normal Defences to UTI (5)

A

o Local IR (resident defense cell . ex macrophages)
o Mucin Layer (glycoprotein produced by cells of bladder wall. Prevents urine from making direct contact with wall (prevents bacteria from making contact)
o Washout (strong urine stream flush urethra)
o Prostatic fluid (anti-microbial properties and some present in urine)
o Women have periurethral normal flora

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5
Q

Three ways fluid transfer between blood and filtrate

A

Auto filtration, active secretion, and reabsorption

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6
Q

Why are women at higher risk of UTI

A

Women have periurethral normal flora

Proximity to anus

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7
Q

Key risk associated with Lower UTI

A

• Catheterization
• Obstruction
o Stasis (loss of washout)
o Reflux

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8
Q

MNFTS of Lower UTI

A
  • Acute Onset
  • Frequency
  • Dysuria
  • Lower Abd/back pain
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9
Q

Dx and Tx of Lower UTI

A

DX
• Mnfts
• Urinalysis

TX
• Start on ABX (pre Dx return)
   o Change if bacteria different then expected
• Tx underlying cause
• If untreated will continue to ascend
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10
Q

What is Pyelonephritis ?

Types) (Common Et

A
  • Inflm of tissue surrounding Renal Pelvis and Parenchyma
  • Upper UTI
  • Acute and chronic Forms

ET
• Various Bacteria
o E coli common (proximity to anus)

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11
Q

What are some common Risks related to Pyelonephritis

A
  • Suppressed Immunity (Most chronic diseases, Diabetes particularly)
  • Catheterization
  • Urinary reflux (BPH
  • Diabetes
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12
Q

Describe a simple Pathology of Pyelonephritis

A
• Ascending infection and Inflm
• Urethra->bladder->Ureter-> Kidney
• Fibrosis and scar tissue (in kidney)
   o Dec renal Function (lots of systemic Fx reduced)
• Chronic form
   o Recurrent Inflm -> renal failure
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13
Q

Describe MNFTS and Tx of Pyelonephritis

A
MNFTS
•	Acute onset
•	Lower back pain
•	Fever (Likely systemic MNFTS)
•	Dysuria, Frequency, Urgency
•	Pyuria (pus in Urine)
•	Severe HTN (chronic form)

Tx
• Abx (10-14days)

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14
Q

Briefly describe the categories of Glomerulonephritis

A

1) Nephrotic Syndrome
• INC Glomerular permeability
o Fluid and protein loss

2) Nephritic Syndrome
• DEC glomerular Permeability
o Fluid and nitrogenous waste retention

3) Sediment Disorders (Whatever settles out of urine)
• hematuria, proteinuria

4) Rapidly Progressive Glomerulonephritis (OUR FOCUS)
• NOTE: Porth terminology is different. Also This is one type of many, but main one that can be extended to understand others

NOTE: These can be mixed and overlap with several of the same features happening at once

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15
Q

Glomerulonephritis

A

Glomerulonephritis
• Glomerular Inflm (r/t Type lll H)
• Several Types
(focus on Acute post infectious (proliferative) GN in Porth)

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16
Q

Describe a Type 3 H

A

Normally: Ab +Ag -> AbAg (IC) is destroyed in blood

  • Type3 H- IC are not destroyed by enzymes as normal-> into blood stream-> enter cap-> embed in Cap wall (throughout body and also in Kidneys)
  • Impedes filtration + abnormal deposit (macrophage will destroy deposit) = Inflm
  • Type 3 H is generally proceeded by infection
17
Q

Describe the Basic of Acute Post-infectious (proliferative) GN

(Et, Timeline, At risk Groups and Prognosis)

A

• Common form
• Preceded by Beta hemolytic strep infect
o Pharynx or skin (7-12 d)
• Mostly in children (95% recover fully)
o Also occurs in Adults (30% end with renal failure
• Type lll hypersentivity: IC traps in glomerulus -> Glomerular filtration (GF) impeded

18
Q

Describe two key characteristics of GN at the level of the glomerular Capsule

A

o Hyper cellularity (leukocytes, mesangial and endothelial)
• Similar to hyperplasia
• NOTE: Unknown why hypercellularity happens, but it is compensatory

o Glomerular Enlargement (make sense r/t Inflm of large number of capillaries)

19
Q

What are the MNFTS of the GN ?

A

Oliguria followed by proteinuria and hematuria
o Proteinuria- holes creates by damage caused by inflm cells clearing capillaries
o Hematuria- Damage capillaries= bleeding

ALSO:
• Inc in BUN and Creatinine (azotemia – nitrogenous waste in blood stream)
• Na and water retention
• HTN and Edema (r/t inc hydrostatic pressure (fluid) and proteinuria)

20
Q

Tx of GN

A
  • Symptomatic Tx (e.g Inflm, azotemia, etc)

* Most are self limiting (beginning of recovery ~2wks from onset)

21
Q

Describe Nephrolithiasis

A

Renal Calculi

  • Kidney Stones-usually develop in the kidney and then migrate out
  • Refers to stones anywhere in Urinary tract
  • Inc incidence in Men
  • Form in kidney -> migration -> obstruction
22
Q

ET of Nephrolithiasis

A

• Complex interaction
• Humans are able to concentrate urine (hypo or hypertonic)
• Diet determines largely what kidneys are required to excrete
o Str changes in Urinary Tract
o Inc concentration in blood/ urine components
o Dietary and metb factors

23
Q

Patho of Nephrolithiasis

A

• Kidney proteins inhibit crystallization (mechanism unknown)
• Defensive vs offensive factors balance
• High [solute] And/or Urine stasis -> precipitators in urine-> nucleus -> crystallization
• 4 types of stones (table 33-2)
o identification may lead to understanding of dietary component responsible
o ex. Stag Horn Calculus

24
Q

MNTFS of Nephrolithiasis

A

• Severe renal colic (min to days) (++PAIN)
o r/t to Supine position, night time
o distended ureter (migration)
o Could also be in urethra
• Non colicky pain
o Distension of renal pelvis and Calyces
• Nausea, vomiting, diaphoretic (all r/t pain)

25
Q

Dx of Nephrolithiasis

A
  • Pain (non migratory, severe)
  • US or CT
  • Urinalysis
  • IVP (intravenous pyelogram [renal pelvis])
  • Dye moves through blood stream into urinary tract until it hits obstruction
26
Q

Tx of Nephrolithisasis

A
  • Pain (opioids, gravol)
  • 90% passed spontaneously (if less then 5mm)
  • Narcotics and antispasmotics (Buscopan)
  • Cause
  • Inc fluid intake
  • Sx? Sounds wave (lithotripsy), caution in breaking up stones
27
Q

Describe three types of Urinary incontinence

A

• Stress incontinence
o Weak sphincter
o Increased intra-abdm pressure (coughing, laughing)
o Urethro-vesicular angle change (more female post childbirth)

• Overflow incontinence (bladder wall transitional epithelial tissue)
o intravesicular pressure > urethral pressure
o Retention and bladder distention

• Overactive bladder
o Hyperactive detrusor muscle ( Neurogenic or myogenic problem)

28
Q

Tx for Urinary incontinence?

A

• Drugs (fortify sphincter) Alpha adrenergic agonist
• Sx (may be required- theres a diversity)
o Prosthesis in severe cases

29
Q

Describe Acute Renal Failure

Key MNFTS and Dx Measures

A
• l/o of renal fx (produce urine)
   o fluid and electrolyte imbalance
   o Azotemia
• Usually reversible (not necessarily self limiting)
• GFR Decrease (hr or days)
• 400ml urine/day to prevent azotemia
• Oliguria: 100-400ml/day 
• Anuria: Less then 100mls per day
30
Q

Describe the 3 possible Etiologies of ARF

A

• Prerenal (majority)
o Hypotension and hypovolemia (dehydration)
o Dec renal perfusion -> oliguria and ischemia

• Intrarenal
Stones, Inflm, GN

• Post Renal
o Eg BPH
o Obstr to urine flow

31
Q

3 phases of ARF

A

o Initiating phase
• Precipitating event to MNFTS onset

o Maintenance phase (maintenance of problem)
• Dec GFR, Oliguria, azotemia

o Recovery
• Tissue repair -> gradual inc in GFR

32
Q

3 MNFTS of ARF

A
  • Oliguria or Anuria (some forms excessive or normal output)
  • Fluid and Electrolyte imbalance
  • Azotemia
  • PLUS Edema, HTN, Proteinuria, hematuria
33
Q

Tx of ARF

A

• Reversible (not self limiting, requires active stat intervention)
• Replace fluids and electrolytes (monitor!)
o Kidneys are not correcting with adjustments, administration needs to be precise.
• Dialysis
o Hemodialysis- channeling blood through machine
o Peritoneal Dialysis- peritoneal membrane richly vascularized
o Diet (well balanced + dec proteins, and low salt)

34
Q

What is Chronic Renal Failure

Describe 3 stages

A
  • Progressive permanent damage
  • Via stages (separate from previously discussed stages)o
o	Diminished renal reserve (fx)
   • GFR  less then 50% OF NORMAL (N=120-130ml/min)
   • No signs of ↓ renal fx
o	Renal Insufficiency
   • GFR 20% -50% of normal
o	Renal Failure
   • less then 20% 
   • Not until 5% that kidney stop functioning completely