This document discusses urinary tract infections (UTIs) and related topics. It begins by describing pyelonephritis, an ascending urinary tract infection that reaches the kidneys. It then covers the signs, symptoms, and laboratory findings of acute pyelonephritis. Chronic pyelonephritis is also discussed. Additional sections cover night sweats, tuberculosis, referred pain, urine analysis, and hematuria.

1. Case 2 - UTI
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 Pyelonephritis
o Ascending urinary tract infection
 Reaches Pyelum of kidney
o Dividing into: A) Acute Pyelonephritis B) Chronic Pyelonephritis
 Acute pyelonephritis (APN)
 Epidemiology:
i. More common in women than men
o Women have a short urethra
 Risk Factors:
i. Urinary Tract Obstruction
ii. Medularry Sponge kidney
iii. Diabetes mellitus
iv. Preganancy
v. Sickle cell trait/disease
 Pathogenesis:
i. Vesicoureteral reflux (VUR) with ascending infection
o Intravesical portion of the ureter is normally
compressed with micturition
 Prevents reflux of urine into the uterus
o In VUR, the intravesical portion of the ureter is not
compressed during micturition
 Urine refluxes into the ureters
ii. Ascending Infection:
o Most common mechanism for UTI in females
o Distal urethra and vaginal introitus are normally
colonised by E. Coli
o Oragnisms ascend into urethra and bladder
 Causes urethritis and cystitis
o If VUR is present, infected urine ascends to the renal
pelvis and renal parenchyma
 Causes APN

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 Gross and microscopic findings:
i. Greyish white areas of abscess formation are in the cortex +
medulla
ii. Microabscess formation occurs in the tubular lumens and
intersstitium (Shown below)
 Clinical Findings:
i. Spiking fever, flank pain
ii. Increased frequency of urination
iii. Painful urination (dysuria)
 Laboratory findings:
i. WBC casts (key fidning)
ii. Pyuria
iii. Bacteriuria (usually E. Coli)
iv. Haematuria
 Complications:
i. Chronic pyelonephritis
ii. Perinephric abscess
iii. Renal Paillary necrosis
iv. Septicemia with endotoxic shock

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 Chronic Pyelonephritis (CPN)
 Pathogensis:
i. VUR starting in young girls
ii. Lower urinary tract obstruction
o Produces hydronephrosis
o Example:
 Prostatic hyperplasia
 Renal stones
 Gross and microscopic findings:
i. Reflux type of CPN
o U-shaped cortical scars
 overlying a blunt calyx
o Visible with
 an intravenous pyelogram (IVP)
ii. Obstruction type CPN
o Uniform dilation of the calyces
o Diffuse thinning of cortical tissues
iii. Microscopic findings
o Chronic inflammation
 Secondary scarring of the glomeruli
o Tubular atrophy
 Tubules contain:
 Eosinophilic material
o Resemble thyroid tissue
‘’Thyroidization’’
Note here the changes we call
"thyroidization." You will see many
chronic inflammatory cells in the
interstitial tissue and dilated tubules
containing pink staining proteinaceous
goo, giving the appearance of thyroid
colloid. You should note the scarring in
the interstitial tissue in general and to
some degree around the glomeruli.
This is often associated with chronic
ischemic injury of the kidney, which
worsens as the process proceeds.
Think diabetes and hypertension.
Reference:
http://medsci.indiana.edu/c602web/602/
c602web/renal/slide79.htm
 Clinical and laboratory findings

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i. History of recurrent APN
ii. May cause hypertension
o Reflux nephropathy is a cause of hypertension in
children
iii. May cause Chronic Renal Failure (CFR)
 Night Sweats:
o There is no good evidence based diagnosis answer
 Due to the following:
i. Limited number of studies on subjects with such ailment
ii. No clinical trial have directly studied symptomatic relief of
night sweats alone
iii. History taking is the best initial diagnostic tool ( Strength of
recommendation (SOR): C, based on usual practice and clinical
opinion)
 Very common complaint for:
i. Menopausal women with hot flashes
ii. Most common age group in both genders (41-55 years)
iii. Common causes not widely studies, mainly attributed to
lymphoma, TUBERCOLOSIS, and HIV infection.
o Not common in outpatient care!
iv. Medications, such as:
o Antidepressant (SSRIs, Venlafaxine... etc.)
o Antimigranes
o Antipyretics (Aspirin, acetaminophen, and NSAIDS)
o Cholinergic agonists
o GNRH agonists
o Hypoglycaemic agents
o Sympathomimetic agents
o Others, alcohol, beta blockers, and calcium channel
blockers to name a few!
 Differential diagnosis:

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 Tuberculosis (TB)
o Epidemiology and pathophysiology:
 Contracted by inhalation of Myobacterium tuberculosis
 Characteristics:
i. Strict aerobe, acid fast (due to mycolic acid in cell wall)
 Screening:
i. Purified Protein derivative (PPD) intradermal skin test
o Does NOT distinguish active from inactive disease
 Primary TB:
i. Subpleural location
o Upper part of the lower lobes or lower part of the upper
lobes
ii. Usually resolves
o Produces a calcified granuloma or area of scar tissue
o May be a nidus for secondary TB
 Secondary (reactivation) TB:
i. Due to reactivation of a previous primary TB site
ii. Invovles one or both apices in upper lobes of respiratory lung

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o Ventilation (oxygenation) is greatest in the upper lobes
o Decrease incidence of TB in mountain people
 Used to be previous treatment before advent of
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strong antibiotics
 Increased antibiotics resistance M. TB
strains brought back mountain less
oxygenation regimen
o Cavitary lesion due to release of cytokines from
memory T Cells
iii. Clinical findings:
o Fever
o Drenching night sweats
o Weight loss
iv. Complications:
o Miliary spread in lungs due to invasion into the
bronchus or lymphatics
o Miliary spread to extrapulmonary sites
 Due to invasion of pulmonary vein tributaries
 Kidney is the most common extrapulmonary site
 Also called: tuberculosis cutis acuta
generalisata
o Massive hemoptysis
o Bronchietctasis
o Scar carcinoma
o Granulomatous hepatitis
o Spread to vertebra (Pott’s disease)
 Referred Pain:

7. Case 2 - UTI
o Pain originating in a visceral structure may be referred to and felt in a somatic
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structure
o Several proposed theories in explaining its mechanism
i. Convergence – projection theory of visceral pain
o Suggest that two different afferent segments terminate
at the same spinal cord level and end there.
o Converging nociceptive inputs into same synaptic
interneuron or second order neuron
o Transmitted to higher brain centers through the same
dorsal horn and intermediate grey matter
ii. Concept of referred pain
o Second order GSA are continuously being activated by
GVA first order neurons
o Thereby, lowering threshold of stimulation of 2nd order
neurons
o Nociceptive inputs is relayed to its somesthetic cortex
o It normally receives normally somatic information from
other areas, such as upper limb
o The brain interprets such information as if it was
coming from somewhere else
o Thus, it’s a problem of the terminal end (i.e.,
somatosensory cortex) that interprets the signals not the
stimulus or receptor that establish localisation of such
sensations
 None Proven to be true!!!
o Still unknown
o Expanded interest in research after World War II
 Due to
i. Generalised painful sensations from phantom limb pain of
soldiers
ii. Increased incidence of myocardial infarcts with the blooming
economic prosperity
o Been known as early as 1880’s
o Best example: Angina pectori
i. Pain sensation arising in heart muscle
ii. Experience as pressure in chest, back , arm
iii. All from regions served by the same segmental spinal nerve
o Can be manifested as a toothache, and neck pain
 Due to same embryological loci derivation
 Patients may visit a dentist, but they
have underlying heart problems
 GO TO A CARDIOLOGIST!!!
o Other areas (related to the case):
i. Suprapubic pain: Prostate hyperplasia

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ii. left flank tenderness : pylonephrititis
 Urine analysis:
o Gold standard in initial work up of kidney function
 A diagnostic tool
i. Ordered at intervals as a rapid method
o Helps monitor organ’s
 Function
 Status
 Response to treatment
ii. Commonly ordered due to UTI’s symptomps:
o Abdominal pain
o Back pain
o Dysuria, or frequet urination
o Haematuria
iii. Can be useful in monitoring certain conditions
o Interpretation of the results:
i. Visual examination:
o Urine colour, clarity, and concentration
 Normal: shades of yellow
 From very pale to dark amber

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o Sometimes blood can contaminate it
 Due to
 haemorroids
 Woman’s mensturation
 Other causes (many pathologic)
o Depth of urine:
 Crude indicator of its concentration
 Pale yellow or colourless
 Diluted urine (aka, water loss)
 Dark yellow
 Concentrated highly osmotic urine
o Seen In first morning urine
o With dehydration
o Or during a fever
o Clarity
 Different termss:
 Clear
 Slighly cloudy
 Cloudy
 Turbid
 Normal: clear or cloudy
 Substances can cause cloudy urine
o Prostatic fluid
o Sperm
o Mucous
o Cells from skin
o Normal urine crystals
 Or Bacteria needs attention!!
ii. Chemical examination:
o Using prepared test strips
 Normal plastic strips holding small squares of
test pads paper
 They absorb urine once dippped
 Chemical reactionoccurs
 Pad colour changes within seconds to
minutes
 Timing is important in diagnosis
 May result in errors
o Best use automated instruments
to read
 Change of colour approximated amount of
existing substance
 Example:

10. Case 2 - UTI
o Slight color – small [protein]
o Dark color - large [protein]
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o Frequent chemical tests:
 Specific Gravity:
 Indicates urine concentration
o No abnormal values
 Comparison between dissoloved
substances and water
 Test pad
o Upper limit (1.035)
o Lower limit (1.002)
 Underlying causes:
o Lack of concentration and
dilution (e.g., CRF)
o First sign of intrinsic renal
disease
 pH:
 No abornamal values
 Indicates acidic or alkaline pH
 Determined by:
o Diet
- Low carb diet = Alkaline
- High protein diet = Acidic
o Proteus infection:
 Alkaline urine, urease
converts urea into
ammonia
 Can cause crystals due to acidity or
alkalinity
o Crystals forming in kidney, are
called ‘’calculus’’
 Protein:
 Elevated in urine, proteinuria
o Early sign of kidney disease
o Normal, little or no protein
 Detects albumin (not globulins)
 SSA: detects albumin and globulins
 Albuminuria: dipstick and SSA have
same results
 Disorders that cause it:
o That can cause high protein level
in blood

11. Case 2 - UTI
o Disorders causes destruction of
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RBC’s
o Inflammation
o Vaginal secretion that get into
urine
 Glucose:
 Not normally present in urine
 When present, called: glucosuria
 Results from:
1) Excessive high glucose level in
blood, diabetes militus
2) Reduction in renal threshold, normal
pregnancy and glucosuria
 Ketons:
 Not normally found in urine
o Intermediate products of fat
metabolism
 Present in high amounts, called:
ketonuria
 Can be an early indication of insufficient
insulin
 Causes:
o Diabetic ketoacidosis
o Starvation
o Ketogenic diets
o Severe exercise
o Exposure to cold
o Carbohydrates loss, (frequent
vomitting)
 Test only detects acetone and AcAc (not
β-OHB)
 Blood:
 Always pathologic in urine
 Sometimes chemically can be negative,
but microscopically found positive
o When it happens
 We test for ascorbic acid (
vitamin C)
 It results into falsely low,
or falsely negative
 High levels are called:
o Hemoglobinuria

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o Hematuria
o Or Myoglobinuria
 Underlying causes:
o Intravascular haemolytic anaemia
o Renal calculus
o Infection
o Cancer
o Crush injuries
 Discussed later in more details, under
Haematouria section
 Leukocyte esterase:
 An enzyme present in WBC’s
 Normally there are few WBC’s in urine
o High levels, will result in this
screening test positive
 Presence of esterase in neutrophils
(pryuria)
 Sterile pryuria (neutrophils present but
negative standard urine culture)
 Underlying causes:
o Infection
o Chlamydia trachomatis urithritis
o Renal tuberclusis
 Nitrite:
 Bacteria convert nitrate into nitrite in
urine
 When bacteria present, they cause UTI,
leading to increase of nitrites
 Postive test is an indication of UTI
 Underlying cause:
o Nitrate reducing uropathogens
ex- E.coli
 Billirubin:
 Not normal present
 Produced by liver from haemoglobin of
dead circulating RBcs
 When present, called: Bilirubinuria
 Underlying cause:
o Viral hepatitis
o Obstructive jaundice
 Urobilonogen:
 Present in urine in low concentration
o Derivavitive of bilirubin

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 Underlying causes:
o Obstructive jaundice
o Viral hepatitis
o Extravascular haemolytic anemia
(e.g., spherocytosis)
iii. Microscopic examination:
o Cells:
 Bacteria
 Red blood cells (hematuria)
 Neutrophils (pyuria)
 Oval fat bodies
 Underlying causes:
o UTI (commonly)
o Renal stones
o Cancers (bladder, renal)
o Infection
o Benign prostatic hyperplasia
o Sterile pyuria
o Renal tubular cells with lipid
(nephrotic syndrome)
o Casts
 Hyaline
 RBC’s
 WBC’s
 Renal tubular cell
 Fatty
 Waxy (refactile, acellular)
 Haematuria
o Definition:
 More than three red blood corpuscles are found in centrifuged urine
per high power field microscopy (>3RBC/HP).
 Aetiology:
i. Diseases of urinary system (most common cause)
o Vascular
 arteriovenous malformation
 arterial emboli or thrombosis
 arteriovenous fistular
 nutcracker syndrome
 renal vein thrombosis
 loin-pain hematuria syndrom
 coagulation abnormality
 excessive anticoagulation
o Glomerular

14. Case 2 - UTI
 IgA nehropathy
 thin basement membrane disease (Alport
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syndrome)
 other causes of primary and secondary
glomerulonephritis
o Interstitial
 allergic interstitial nephritis
 analgesic nephropathy
 renal cystic diseases
 acute pyelonephritis
 tuberculosis
 renal allograft rejection
o Uroepithelium
 malignancy
 vigorous excise
 trauma
 papillary necrosis
 cystitis/urethritis/prostatitis (usually caused by
infection)
 parasitic diseases (e.g. schistosomiasis)
 nephrolithiasis or bladder calculi
o Multiple sites or source unknown
 Hypercalciuria
ii. System disorders:
o Haematological disorders:
 aplastic anemia
 leukemia
 allergic purpura
 hemophilia
 ITP (idiopathy thrombocytopenic purpura)
o Infection:
 infective endocarditis
 septicemia
 epidemic hemorrhagic fever (Hantaan virus)
 scarlet fever (-hemolytic streptococcus)
 leptospirosis (leptospire)
 filariasis (Wuchereria bancrofti, Brugia malayi)
o Connective tissue diseases
 systemic lupus erythematous (SLE)
 polyarthritis nodosa
o Cardiovascular diseases

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 hypertensive nephropathy
 chronic heart failure
 renal artery sclerosis
o Endocrine and metabolism diseases
 gout
 diabetes mellitus
iii. Diseases of adjacent organs to urinary tract
o Appendicitis
o salpingitis
o carcinoma of the rectum
o carcinoma of the colon
o uterocervical cancer
iv. Drug and chemical agents
o Sulfanilamides
o anticoagulation
o cyclophosphamide （CTX)
o mannito
v. miscellaneous
o exercise
o “idopathic” hematuria
 Clinical Features:
i. Colour:
o Depends on
 amount of RBC’s in urine
 Ph value
 Normal:
o Yellow colour
o 6.5
ii. pH:
o Acidic: more darker (brown or black)
o Alkaline: red

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Red urine, indicative of its alkalinity Dark urine, indicative of its acidity
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A) Red cast in urine B) RBC’s in urine

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 Drugs:
o Fluroquinolones:
 1st generation: - Nalidxic acid
 2nd generation :
i. Aprofloxicin
ii. Norfloxicin
iii. Ofloxoicin
 3rd generation: larofloxicin
 4th generation: Moxifloxacin
 Fatal
 Have broad spectrum activity (gram (+) , and gram (-))
 Inhibit DNA replication by interfering with Topoisomerase II, IV
 Drug of Choice:
o For resistant tuberclusis patient
o Isoniazid:
 Prodrug that must be activated by bacterial catalylase
o Enzyme present in M. TB
o Known as kat G.
o Form a complex inhibits fatty acid synthesis
 Decreases synthesised mycolic acid
 No bacterial wall
o Side effects:
 Rash

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 Hepatitis
 Anemia
 Peripheral neuropathy
 Mild CNS disturbances
o Rifampin:
 Inhibit DNA dependant RNA polymerase
o By binding to B-subunit of RNA
o Prevents transcription to RNA
o Thus, no translation to proteins
 Side effects:
i. Hepatotoxicity (most common)
ii. Respiratory distress
iii. Abdominal pain
iv. Nausea
v. Vomitty
vi. Cramps
vii. Diarrhoae
viii. Flue-like syndrome
o Pyrazinamide:
 Prodrug that is a activated by pyrazanmaidase
 Present in M. Tuberclosis
 Forms pyrozonic acid
 Inhibits FAS
 Distubes bacterial wall
 Side effects:
i. Most common: arthlagia
ii. Most severe: hepatotoxicity
o Ethambatol:
 Bacteriostatic
o Obstruct of cell wall synthesis (TB)
o Disturbs arabinogalactin synthesis
 By inhibiting arabynosyl transeferase
 Important in bacterial
wall synthesis
References:
o Robbins
o http://medsci.indiana.edu
o Up-to-date
o http://www.edrep.org
o http://acutemed.co.uk
o http://en.diagnosispro.com/
o http://www.nlm.nih.gov
o http://jfponline.com