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Big Ol' Patho. > Pyelonephritis + UTI + Glomerular Disease > Flashcards

Pyelonephritis + UTI + Glomerular Disease Flashcards

1
Q

Pyo = ?

Pyelo = ?

A 
Pyo = pus
Pyelo = refers to renal pelvis
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2
Q

What is pyelonephritis?

Acute or chronic?

A
  • Upper UTI (in kidney…lower is in bladder)
  • Inflm of renal pelvis & parenchyma
  • Acute + chronic forms
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3
Q

Etiology of pyeloneph?

A
  • D/t various bacteria infection (Usually E. Coli)
  • Risks
  • Suppressed immunity
  • Catheterization
  • Urinary reflux d/t things like BPH
  • DM – infections common
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4
Q

Patho of pyeloneph?

A

• Ascending infection and inflm
o Urethra→ bladder→ ureter→ kidney
• Fibrosis and scar tissue? –> Dec renal Fx

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5
Q

Why scar tissue with pyeloneph? What is this unlike other bacterial infections?

A

• Being bacterial the progression is what we would normally see in the body, with one exception. As it progresses there is scarring within the kidney (dependent on the duration of the infection); often times scarring is NOT fully reversible. This is an issue bc we are replacing fx’al tissue w non-fx’al tissue. If this happens we will have a problem w renal fx

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6
Q

What are the two ways that you end up with the chronic form of pyeloneph?

A

either infection persists, or chronic inflm

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7
Q

Patho of chronic form of PN?

A
  • Recurrent inflm→ obstruction or reflux (reflux from ureter into renal pelvis)
  • Renal damage (irreversible)→renal failure?
  • Remember: infection in a VITAL organ→serious concerns if not treated (Think- scar tissue in heart/liver…big freakin deal!)
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8
Q

Manifestations of PN?

A
  • Bc bacterial→local and systemic mnfst
  • Acute onset
  • Lower back pain
  • Fever
  • Dysuria, freq, and urgency: typical urinary mnfst that appear bc of irritation wi urinary tract
  • Pyuria (pus in the urine from the purulent exudate)
  • Severe HTN (chronic form)
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9
Q

Tx of PN?

A
  • Abx (10-14 days) slightly longer than normal (2x) to ensure all bacteria is eradicated
  • Chronic? Inflm needs to be addressed- anti-inflm
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10
Q

Is URT or LRT infection more common?

A

URT is the most common

LRT second most common infection
of all infections???…

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11
Q

What are the defenses against lower UTI’s?

A

1) Local IR
2) Mucin layer
3) Wash out
4) Prostatic fluid in men
5) Microbial antagonism in women

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12
Q

Mucin layer as protective mechanism against L UTI?

A

bladder wall is made of transitional epi tissue, cells there secrete a glycoprotein that coats the inner layer of epi tissue and forms barrier between urine and epi tissue; prevents direct contract of bacteria

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13
Q

“wash out” as protective measure?

A

voiding urine is a consequential defense mechanism (voiding bacteria as well)

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14
Q

Prostatic fluid + microbial antagonism as mechanisms of protection against l UTI’s.

A

o Prostatic fluid: Men-contains components that anti-microbial (anti-bacterial)
o Microbial antagonism: Women- NF are already occupying the niche in the peri-urethral area

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15
Q

Risks for lower UTI?

A

• Catheterization
• Obstruction
- Stasis- avoiding washout
- Reflux- urine form distal part into bladder carrying microbes along w it

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16
Q

Catheterization as risk for UTI?

A

bacteria attach to catheter and secrete biofilm to anchor them on the catheter

17
Q

Mnfts of lower UTI?

Tx?

A
  • Acute onset
  • Freq
  • Dysuria
  • Lower abd/back pain
  • Abx (will start right away, wont wait for culture, will confirm after)
  • Underlying cause
18
Q

How come human and bird kidneys can produce hypertonic filtrate?

How is filtrate concentration controlled?

A

Loop of Henle

• 3 options: hypertonic urine, hypotonic urine, isotonic urine→all determined on physiological status; our kidneys do this by changing the permeability

19
Q

5 clinical categories of glomerular disease?

A

1) nephrotic syndromes
2) nephritic syndromes
3) sediment disorders
4) Rapidly progressive glomerulonephritis
5) chronic glomerulonephritis

20
Q

Nephrotic syndromes?

A
  • Inc glomerular perm→fluid and protein loss
  • Inc in perm→more components out at the level of the glomerulus. If perm inc we will have more ease of ultra filtration (push out fluids [water + 660s], nitrogenous wastes). Consequence of this is fluid loss and PROTEIN loss (should never appear in urine)
  • This can be physiologic
21
Q

Nephritic syndromes?

A
  • Dec glomerular perm→ fluid and nitrogenous waste retention
  • This is NOT physiologic

When dealing w glomerular disease, often times you have a mix of nephritic and nephrotic features

22
Q

Sediment disorders

A
  • Hematuria, proteinuria: will sediment out

* Mix of both nephrotic and sediment disorders

23
Q

What is glomerulonephritis?

A
  • Glomerular inflm

* Several types (Porth uses complex method- stick w what Ahmed has given us)

24
Q

Acute post-infectious (proliferative) GN

What is this preceded by? Where and for how long?

A

• Preceded to Beta hemolytic strep infection
o Pharynx or skin (7-12 days)
o Most occurs in kids; develop strepp throat or dermal infection
o Beta is not the receptor- referring to type of strepp that causes hemolysis

25
Q

What pop does acute post-inf GN occur in?

How does progress in adults?

A

• Mostly in children (95% recovery)

o Occurs in adults: 30% will progress to renal failure (kids wont)

26
Q

Outline type of hypersensitivity that occurs in Acute PI GN?

A

• Type 3 H: IC traps in glomerulus→GF impeded
o Remember: Type 3 hypersensitivity- Ag+Ab→AbAG (IC)
o IC broken down enzymatically (cleave and recycle); Type 3 H, IC escape E detection (bc they are small or insoluble)→get in capillaries→GN

• Estimated GFR- [creatinine] of blood and urine; we are clogging endothelium w IC→affecting filtration

27
Q

What 2 histological features are characteristic of GN?

Are these easy to explain?

A 
o	Hypercellularity (excess cells: leukocytes, mesangial and endothelial cells)
2) Glomerular enlargement
  • No, are hard to explain
28
Q

Mesangial cells

Why do you see hypercellarity?

A
  • Mesangial cells are in the glomerulus in between neighbouring capillaries
  • Why should these cells be increasing? Damage epi cells you replace them, but with normal numbers, not excessive
29
Q

Why glomerular enlargement in GN?

A

• Inflm→exudate and swelling

30
Q

Manifestations of GN?

Tx?

A

• Oliguria followed by proteinuria, hematuria
- Inc BUN + creatinine
- Na + H2O retention
o Severe HTN (hypervolemia)
o Systemic edema bc of fluid retention and bc or proteinuria (dec OP)

  • Symptomatic tx
    Most are self limiting (wks)
31
Q

Why oliguria followed by proteinuria + hematuria in GN?

A

o Initially you are plugging endothelium, impeding perm. Less fluid goes through, if you dec V of urine (oliguria)
o We have holes which permit large molecules to move through (proteinuria)
o These are capillaries: inflm, damage, bleeding into filtrate, pass through to urine

32
Q

Why Inc BUN + Inc creatinine with GN?

A

o Not able to push out enough fluid, you are retaining N wastes (azotemia)

Big Ol' Patho. (17 decks)

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