Renal Flashcards
Describe Macro Renal Terms-
Hilus
Renal Pelvis
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
Describe Micro Renal terms-
Nephron
Glomerulus
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
Describe Lower UTI
Incidence, infectious agent, from where, progression?
- Common
- Variety of Bacteria (usually E. Coli)
- Urine is sterile, but normal flora in external genitalia
- More common in women
- Ascending infection
Describe our normal Defences to UTI (5)
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
Three ways fluid transfer between blood and filtrate
Auto filtration, active secretion, and reabsorption
Why are women at higher risk of UTI
Women have periurethral normal flora
Proximity to anus
Key risk associated with Lower UTI
• Catheterization
• Obstruction
o Stasis (loss of washout)
o Reflux
MNFTS of Lower UTI
- Acute Onset
- Frequency
- Dysuria
- Lower Abd/back pain
Dx and Tx of Lower UTI
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
What is Pyelonephritis ?
Types) (Common Et
- Inflm of tissue surrounding Renal Pelvis and Parenchyma
- Upper UTI
- Acute and chronic Forms
ET
• Various Bacteria
o E coli common (proximity to anus)
What are some common Risks related to Pyelonephritis
- Suppressed Immunity (Most chronic diseases, Diabetes particularly)
- Catheterization
- Urinary reflux (BPH
- Diabetes
Describe a simple Pathology of Pyelonephritis
• 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
Describe MNFTS and Tx of Pyelonephritis
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)
Briefly describe the categories of Glomerulonephritis
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
Glomerulonephritis
Glomerulonephritis
• Glomerular Inflm (r/t Type lll H)
• Several Types
(focus on Acute post infectious (proliferative) GN in Porth)
Describe a Type 3 H
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
Describe the Basic of Acute Post-infectious (proliferative) GN
(Et, Timeline, At risk Groups and Prognosis)
• 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
Describe two key characteristics of GN at the level of the glomerular Capsule
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)
What are the MNFTS of the GN ?
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)
Tx of GN
- Symptomatic Tx (e.g Inflm, azotemia, etc)
* Most are self limiting (beginning of recovery ~2wks from onset)
Describe Nephrolithiasis
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
ET of Nephrolithiasis
• 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
Patho of Nephrolithiasis
• 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
MNTFS of Nephrolithiasis
• 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)
