Professional Documents
Culture Documents
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Pancreatic Disease
. Body related
posteriorly to left
crus, left adrenal,
left renal vein, and
splenic vein
Celiac Axis (trunk,
artery) lies
superior to body
Acute Pancreatitis
1.
http://www.pathguy.com/~lulo/lulo0028.htm
Pancreatitis
Pathogenesis
1.
2.
3.
4.
5.
Obstruction- Secretion
Common Channel theory
Duodenal reflux
Increased permeability of pancre
atic duct
Enzyme Auto-activation
Pancreatitis
Aetiology I
1.
2.
3.
Gall stone
1.
90% of acute pancreatitis .
2.
Life risk of 3-5%
3.
Age 40s .
4.
F>m
5.
Transient obstruction
Alcohol 75% of chronic pancreatitis
1.
Spasm of the sphinctor of Oddi
2.
Increases the concentration of enzymes
3.
Structural damage caused by the precipitation of calciu
m
4.
Transient reduction of blood flow
Drugs
1.
Steroids, AZT
2.
Sulphonomids, Tetracyclin
3.
Oestrogen
Acute Pancreatitis
Clinical Presentation
Abdominal Pain
Constant, quick onset, variable in severity
Epigastric
Radiating to the back in 50% of patients
Associated with nausea, vomiting & retching
Relieved by lying on to the L side, legs-up
Other precipitating factors
Fever in 70%
Jaundice in 30%
Shock +/_ in 10%
Hematemasis & malena in 5%
Acute Pancreatitis
Clinical Presentation II
Dyspnoea in 10%
Tender Abdomen: Mild to severe
Peritonitis,could be diffuse
BS: hypoactive
Abdominal Mass:
Phlegmon
Pseudocyst,
Abcess Ascitis
Cullens
Gray-turner signs
Erythametous skin lesions
Differential diagnosis
Perforated
DU
Perforated GB
Emphsymatous cholecystitis
Mesenteric infarction
AAA
Others
Acute Pancreatitis
Investigation II
Acute Pancreatitis
Investigation III
Radiological:
Plain X- rays:
Others:
Acute Pancreatitis
Complications II
Systemic
Metabolic
I.
Hypokalaemia, Hypochloraemia
& Metabolic alkalosis
Hypocalcaemia
Hypomagnesemia
Hypoxemia
Acute Pancreatitis
Treatment
I.
II.
Conservative
( Admit in ICU VS Common Surgical Ward)
NBM vs Early nutrition
? NGT
Analgesia: narcotic
Adequate fluid replacement ( Initial crystalloid then colloi
d)
Antibiotics (organisms & penetration)
??Anticholinergics, somatostatin have no proven benifit
Minimally invasive
Early ERCP & sphinctorotmy for impacted stones
CT-guided drainage of Psedocusysts
Treatment II
Surgery is contraindicated in uncomplicated
attacks.
1.
2.
3.
4.
5.
6.
Multiple sump tubes are used after pancreatic surgery. Triple-lumen tubes consist
of ports that provide tubing for irrigation, 18
air venting, and drainage.
Summary of treatment
All
patients
Nasogastric suction
NPO
Monitor and maintenance of intravascular volume
Respiratory monitoring and support
Antibiotics(selective)
Early laparotomy only fordiagnosis
Estimate prognosis by early signs
Patients
Peritoneal lavage
Nutritional support
Suspect and treat pancreatic sepsis
Heparin if hypercoagulable
Pancreatitis
Necrotizing Pancreatitis
Pathophysiology
Disruption in the normal separation of lysosomal
Biliary pancreatitis
obstructing stone at ampulla allows bile to reflu
x into the pancreatic duct
obstructing stone at ampulla produces pancreat
ic duct hypertension
Radiographic studies
Abdominal x-ray
typically nonspecific
may exclude other causes of abdominal pain
may show a sentinel loop or a colon cutoff sign
Ultrasound
typically shows a diffusely enlarged,
hypoechoic pancreas
sensitivity of 67% and near 99% specificity in
the diagnosis of acute pancreatitis
MRCP
Conclusions
Necrotizing
Patients
Surgery
Pancreatitis
Chronic Pancreatitis
e back
Nausea, Vomiting
Severe weight loss when steatorrhoea is p
resent
Overt diabetes mellitus
Pancreatic Tumors
Pancreatic Cancer
CLINICAL FEATURES:
Modes of presentation:
Weight loss
Pain
Jaundice
Steatorrhoea
Diabetes Mellitus
Acute Pancreatitis
Malignant Ascites
Approach to Investigations:
(Selective Investigations)
Ultrasound Scan
C.T. Scan
MR Imaging Scan
ERCP
Pancreatic tumors,
In Body of Pancreas:
a. Gnawing pain radiating to back
b. Pain increases after eating or
lying down
c. Weight loss, anorexia
d. Large tumor may compress IVC,
portal vein
A. Surgical Treatment
B. Non Surgical Treatment
SURGICAL TREATMENT:
Pancreatic
Pancreas Tumors
ENDOCRINE TUMORS:
INSULINOMA:
The commonest islet cell tumour and ari
se from the beta cell and situated anywh
ere on the surface or within the substan
ce of the pancreas.
n
Surgery of the pancreas
includin
g transplantation
Liver Transplantation
for
Alcoholic
Liver Disease
Pancreas
Transplantation
Robotic
Step 3 Hepatic Hilum
Pancreaticoduodenectomy
Splenectomy
Total
gastrectomy
Lung
lobectomy
Colorectal
surgery
Thyroidectomy
Adrenalectomy
Esophagectomy
Major
hepatectomies
CBD Procedures
Whipple
GASTROENTEROLOGY
Small intestine
Made
up of three parts:
ileum, jejunum, and duodenu
m.
Main
function is absorption
bowel disease
bowel obstruction
Cancer of
Diarrhea
It
is a symptom not a p
rimary disorder.
It
Causes:
Bacteria toxins
Parasitic infections
Malabsorption syndro
mes
Medication
Systemic disease
Allergies
Psychogenic
Inflammatory bowel
disease
Nonspecific
ulce
rative colitis (U
C)-RCUH
Crohns disease
(CD)
Crohns disease
Nonspecific ulcerative colitis
Ulcerative colitis
Crohns disease
Localization
of damage
Volume of
damage
Depth of
damage
Ulcerative colitis
(RCUH)
Ulcerative colitis
Affects
Primarily
Ulcerative colitis
Chronic diffuse inflammation of large intestine with
Ulcerative colitis
onset
Attacks last 1-3 months
Occur at intervals of months to years
Diarrhea is the predominant symptoms o
f all types of ulcerative colitis.
Typically
management
Surgical
management
Pharmacological treatment
Sulfasalazine
(Azulfidine) SALAZOPIRI
NA anti-inflamatory
inhibits prostaglandin production in the bo
wel.
Mesalamine
Corticosteroids-anti-inflammatory effects
Use as a treatment during acute attacks.
Crohns disease
Crohns disease
Primarily
rs)
Can
Most
Crohns disease
Cause
Like
is unknown
Pathophysiology of Crohns di
sease
Begins with an aphthoid lesion similar to can
a cobblestone appearance.
a are common.
ery
r fistula formation.
Neoplastic Disorders:Polyps
and Colorectal Cancer
1
Colorectal Polyps
1
Polyps
Polyps are masses of tissues that arise from t
Polyposis
Symptoms of polyps
Most
are asymptomatic
Intermittent
Dark
or bright blood
enema
Sigmoscopy
Digital
examination
Colonoscopy
Once
identify polyps ne
ed to be remove becaus
e of the risk of maligna
ncy.
They can be remove du
ring colonoscopy using
electrocautery snare or
hot biopsy forceps pass
ed through the scope
Colorectal Cancer
APC
loss
Adenoma
K-ras
mutation
Chrom 18
loss
Cancer
p53
loss
Normal
HyperEarly Intermediate Late
Cancer
Epithelium proliferation Adenoma Adenoma Adenoma
>50 years
Polyps
Cancer elsewhere in
Family
the body
Hx of colorectal cancer
Ulcerative
Rectum
Bleeding
Altered bowel habi
t
Tenesmus
Pain
Bladder symptoms
Chemotherapy
djunct)
Laparoscopic Resection
Radiation therapy
While
radiation ther
apy is not effective as
a primary treatment
for colon cancer it is
recommended as adj
unct therapy speciall
y for rectal tumors.
Small
rectal cancer
may be treated with i
ntracavitary, externa
l,or implantation rad
iation.
Radiation
reduce the
recurrences of rectal
and pelvic tumors
Gata????
NEPHROLOGY- I
Prof univ dr Ion C Tintoiu
Renal cortex
Cortical lobules - which
form caps over the
bases of the pyramids
Renal columns - which
dip in between the
pyramids
Renal medulla
has 10 conical masses
called renal pyramids,
their apices form renal
papillae
Renal sinus
Space that extends into kidney from hilus
Contains branches of renal artery and renal vein
Renal pelvis divides into 2-3 major calices and these in turn divide into 713 minor calices, each minor calyx (cup of flower) ends in an expansion
which is indented by 1-3 renal papillae
-Nephron
struc
and
Functions
Glomerulus
Proximal Tubule (PCT)
Loop of Henle
Distal tubule
Collecting tubule
Secretion
Excretion
Glomerular Filtration
Figure 26.10a, b
Loop of Henle
Reabsorbed
water reabsorption is passive and follows
concentration and osmotic gradients (except thick
ascending loop)
Sodium reabsorption is coupled to both K+ and Clreabsorption
Cl- in tubular fluid is rate limiting factor
Calcium and magnesium reabsorption
Parathyroid hormone calcium reabsorption at this
site
Loop diuretics inhibit Na and Cl reabsorption in TAL
compete with Cl- for its binding site on carrier protein
Distal tubule
Very tight junctions between tubular cells
relatively impermeable to water and Na+
5% of filtered Na+ load reabsorbed
Parathyroid hormone and vit D mediated
calcium reabsorption
The late distal segment (collecting segment)
Hormone
Collecting tubule
5-7%
Nephron symphony
. Renal
Pathology
4-Urinary obstruction
Stones
Hydronephrosis
5- Cystic diseases of the ki
dney
6-Tumors
Benign
Malignan
7-Litiazis
Glomerular diseases
GLOMERULONEPHRITIS
Acute
Glomerulonephritis:
Rapidly Progressive Glomerulonep
hritis
Chronic Glomerulonephritis
Nephrotic Syndrome
Asymptomatic urinary abnormalit
ies
Glomerular disease
Primary Glomerulonephritis
Minimal change GN
Membranous GN
Focal segmental GS
Membranoproliferative GN
Diffuse proliferative GN
Crescentic GN
Secondary Glomerulonephritis
Diabetes
Vascular disease
atherosclerosis
HTN
Vascultitis
SLE, DM, Amyloidosis, Goodpasture
Hereditary Albort syndrome
Glomerular diseases:
Primary Glomerulonephritis
. Acute
Glomerulonephritis
Acute Glomerulonephritis
Definition
Acute glomerulonephritis is the inflammatio
n of the glomeruli which causes the kidneys
to malfunction
It is also called Acute Nephritis, Glomerulo
nephritis and Post-Streptococcal Glomerulo
nephritis
Predominantly affects children from ages 2
to 12
Incubation period is 2 to 3 weeks
Acute Glomerulonephritis
General Symptoms
Fever
Headache
Malaise
Anorexia
Nausea
and vomiting
High blood pressure
Pallor due to edema and/or anemia
Confusion
Lethargy
Loss of muscle tissue
Enlargement of the liver
Acute Glomerulonephritis
Acute Glomerulonephritis
Etiology
Infectious
Streptococcal
Nonstreptococcal postinfectious glomerulo
nephritis
Bacterial
Viral
Parasitic
Noninfectious
Multisystem systemic diseases
Primary glomerular diseases
Acute Glomerulonephritis
INVESTIGATIONS
- Urea
- Creatinine
- Urinalysis (MSU):
a) Urine microscopy (red cell
cast)
b) proteinuria
Acute Glomerulonephritis
Complications
Hypertensive
encephalopathy,
Heart failure and acute
Pulmonary edema may occur in severe
cases
Acute
Acute Glomerulonephritis P
revention
proper hygiene
prompt
Treatment
Treat the underlying infections when acute GN is associated with chronic infections.
Antimicrobial
therapy
Antibiotics (eg, penicillin) are used to control local symptoms and to prevent s
Loop
diuretic therapy
Loop diuretics may be required in patients who are edematous and hypertens
Diet:
Sodium and fluid restriction
Protein restriction for azotemic patients
Activity: Recommend bed rest until signs of glomerular inflammation and cir
culatory congestion subside.
Chronic glomerulonephritis
Chronic glomerulonephritis
The condition is characterized
1 - irreversible and progressive glomerular a
nd tubulointerstitial fibrosis
2-ultimately leading to a reduction in the glo
merular filtration rate (GFR) and
3- retention of uremic toxins
.
. The diagnosis of CKD can be made without
knowledge of the specific cause.
Chronic glomerulonephritis
Etiology
Nearly all forms of acute glomerulonephritis have a t
endency to progress to chronic glomerulonephritis.
The progression from acute glomerulonephritis to ch
ronic glomerulonephritis is variable.
Whereas complete recovery of renal function is the r
ule for patients with poststreptococcal glomerulon
ephritis, several other glomerulonephritides,
such as immunoglobulin A (IgA) nephropath
y, often have a relatively benign course and many
do not progress to ESRD.
Chronic glomerulonephritis
Pathogenesis
Reduction in nephron mass from the initial injury re
duces the GFR.
This reduction leads to hypertrophy and hyperfiltrat
ion of the remaining nephrons and to the initiation
of intraglomerular hypertension.
These changes occur in order to increase the GFR of
the remaining nephrons, thus minimizing the func
tional consequences of nephron loss.
The changes, however, are ultimately detrimental be
cause they lead to glomerulosclerosis and furt
logic Findings
In early stages, the glomeruli may still sh
ow some evidence of the primary diseas
e.
In advanced stages, the glomeruli are hy
alinized and obsolescent.
The tubules are disrupted and atrophic,
and marked interstitial fibrosis and art
erial and arteriolar sclerosis occur.
Chronic glomerulonephritis Hi
stologic Findings
1-Minimal-Change Disease
2-Focal segmental glomerulos
clerosis
3-Mesangiocapillary GN
4-Membranous nephropathy
Chronic glomerulonephritis
Minimal change Disease
Membranous Nephropathy
thickened BM, IF +ve for IgG & C3 and
subepithelial deposits on EM
cal Manifestations
Uremia-specific findings
Edemas
Hypertension
Jugular venous distension
overload is present)
Pulmonary rales (if pulmonary edema is pr
esent)
Pericardial friction rub in pericarditis
Tenderness in the epigastric region or blood
in the stool (possible indicators for uremic g
astritis or enteropathy)
Chronic glomerulonephritis
Lab Studies
Urinalysis
Urinary protein excretion
Serum chemistry
Serum creatinine and urea nitrogen levels a
re elevated.
Impaired excretion of potassium, free water, and a
cid results in hyperkalemia, hyponatremia, and lo
w serum bicarbonate levels, respectively.
Impaired vitamin D-3 production results in hypoc
alcemia, hyperphosphatemia, and high levels of pa
rathyroid hormone.
Low serum albumin levels may be present if uremi
a interferes with nutrition or if the patient is nephr
otic.
ng Studies
Renal
ultrasonogram
Obtain a renal ultrasonogram to dete
rmine renal size, to assess for the pre
sence of both kidneys, and to exclude
structural lesions that may be respon
sible for azotemia.
Small kidneys often indicate an irrev
ersible process.
Kidney biopsy
ment
ent
Minimal change glomerulonephritis
1-Corticosteroids induce remission in >90% of
children and 80% of adults (slower response).
2-immunosuppression: (cyclophosphamide, ci
closporin (=cylosporin)): early/ frequent relapses;
steroid SEs/dependence.
Prognosis: 1% progress to ESRF.
ment
Focal segmental glomerulosclerosis
Poor response to corticosteroids (1030
%). Cyclophosphamide or ciclosporin (=cyl
osporin) may be used in steroid-resistant cases.
Prognosis: 3050% progress to ESRF.
ment
Mesangial proliferative GN
1-Antibiotics,
2-Diuretics, and
3-Antihypertensives as necessary.
4-Dialysis is rarely required.
Prognosis: Good.
ment
Membranous nephropathy
If renal function deteriorates, consider corti
costeroids and chlorambucil. Prognosis: U
ntreated, 15% complete remission, 9% ESR
F at 25yrs and 41% at 15yrs.
. Rapidly Progressive
Glomerulonephritis
iology
The cause of RPGN is unknown. A geneti
c predisposition may exist for the devel
opment of this disease.
Multiple studies have demonstrated that
ANCA- (antineutrophil cytoplasmic an
tibodies) activated neutrophils attack v
ascular endothelial cells.
ANCA-associated vasculitis.
A viral etiology is possible.
Pathology
Renal biopsshow
A diffuse, proliferative, nec
rotizing glomerulonephri
tis with crescent formatio
n.
The main pathologic findin
g is fibrinoid necrosis (>9
0% of biopsy specimens);
extensive crescent format
ion is present in at least 5
0% of glomeruli.
Clinic
al Manifestations
Symptoms
e,
pain,
haematuria,
systemic symptoms (fever, malaise,
myalgia, weight loss).
b Studies
eatment
1-High-dose corticosteroids; cyclo
phosphamide plasma exchang
e/ renal
2-Transplantation.
Prognosis:
Poor if initial serum creatinine
>600mol/L.
Nephrotic syndrome
Generalized
Oedema
DAMAGED
Proteinuria
Nephrotic syndrome
Etiology
Primary (idiopathic):
Minimal change disease
Most common cause in children
Membranous Nephropathy
Most common cause in Adults
Focal Segmental Glomerulosclerosis
MembranoProliferative Glomerulonephr
itis
Secondary to:
DM (the leading cause of secondary nephrotic syndrome)
SLE
Amyloidosis
Infections:
Hepatitis B and C, HIV,syphilis, post-streptococcal
Malignancy:
multiple myloma , Hodgkin lymphoma, solid tumor
Drugs
(NSAIDs, gold, penicillamine ,heavy metals etc).
Nephrotic syndrome
Clinical Presentation
Generalized Odema
-The predominant feature
-The face, particularly the
periorbital area, is swollen
in the morning& lower extremities
and genital area later in the day
-In advanced disease: the whole body
(anasarca) shortness of breath
Frothy urine and urine dipstick
proteinuria value of 3+
Symptoms & signs for secondary
Nephrotic syndrome
Diagnostic
Renal biopsy
Nephrotic syndrome
Treatment
ms
o
t
p
sym
Compli
cation
Diseasespesific
162
Management of symptoms
Oedema
Low salt diet
Diuretics
serial measurement of body
weight
Proteinuria
ACE inhibitors or ARBs
Hypoalbuminaemia
Management of complication
Hyperlipidaemia
Regular Lipid profile
Statin if severe long lasting nephrotic
syndrome
Control other CVD risk factorstarget blood
pressure 125/75
Thromboembolic risk
Infections
High index of suspicion
Antipneumococcal
and influenza
Ref:
Up to date online 17.3.
60 mmol/24 hrs
water restriction
diuretics (if not volume depleted)
reduced protein diet (controversial)
treat infections
prophylaxis for thrombosis
specific therapy
corticosteroids
Immunosuppression
Diabetic Nephropathy
aggressive glucose control and aggressive BP control
with ACE
Nu s-a terminat !
NEPHROLOGY-II
Prof univ dr Ion C Tintoiu
1-Interstitial Nephritis
2-Diabetic Nephropathy
3-Microscopic Vasculitis and SLE
4-Gout and the Kidney
5-Myeloma Kidney
1-Interstitial Nephritis
infiltration
Mechanical
fenoprofen <1%
frusemide <1%
bumetanide <1%
cimetidine <1%
allopurinol <1%
5 aminosalicylates
ranitidine (rare)
Bacterial infection
bacterial
Autoimmune
systemic
lupus ery
thematosus
transplant rejectio
n
deposition
of :
calcium salts
uric acid
and leukaemias
myeloma
Bence-Jones protein (light chains from maligna
nephropathy
calculi
ureteric
fibrosis
prostatic hypertrophy
urethral stenosis
tumours
(50%)
proteinuria (~1-2 g/24hrs)
reduced urinary concentrating ability
salt wasting
renal tubular acidosis
renal impairment
inactive urine sediment common (cf nephritis)
eosinophils in urine and interstitium in acute hypersens
itivity reactions
renal biopsy
improvement after withdrawal of drugs and toxins
use
of corticosteroids (prednisone)
water and and electrolyte
treatment of hypertension
2-Diabetic nephropathy
Diabetic Nephropathy
Pathological lesions:
diffuse glomerular sclerosis
nodular sclerosis (Kimmelstiel -Wilson lesion)
arteriolar hyalinisation
Associated lesions:
Papillary necrosis
Pyelonephritis
Bladder dysfunction
Radio contrast renal failure
hyporeninaemic hypoaldosteronism with hyperkalae
mia
. 3- Lupus Nephritis
Vasculitis
ype V : membranous
Type IV : diffuse
proliferative
WHO classification
Type II : mesangial
Lupus nephritis
Hematuria
and proteinuria
HTN common
Active urine sediment: rbc casts
Decreased C3 and C4
anti-double stranded DNA antibody specific for
active nephritis
Prognosis varies greatly based on initial pathol
ogy, usually guarded
Treatment
NEPHROLOGY-III
Prof univ dr Ion C Tintoiu
n
the failure of the kidney to excrete nitrogenous waste products
and
to maintain fluid and electrolyte homeostasis
ARF Rapid deterioration of renal function
(increase of creatinine of >0.5 mg/dl in <72hrs.)
azotemia (accumulation of nitrogenous wastes)
elevated BUN and Creatinine levels
decreased urine output (usually but not always)
Oliguria: <400 ml urine output in 24 hours
Anuria: <100 ml urine output in 24 hours
Pre-renal
Volume depletion
Renal losses (diuretics, polyuria)
GI losses (vomiting, diarrhea)
Cutaneous losses (burns, Stevens-Johnson syndrome)
Hemorrhage
Pancreatitis
Decreased cardiac output
Heart failure
Pulmonary embolus
Acute myocardial infarction
Severe valvular heart disease
Abdominal compartment syndrome (tense ascites)
Renal
Glomerular
Antiglomerular basement membrane (GBM) disease (Goodpasture syndr
ome)
Antineutrophil cytoplasmic antibody-associated glomerulonephritis (AN
CA-associated GN) (Wegener granulomatosis, Churg-Strauss syndrome, m
icroscopic polyangiitis)
Immune complex GN (lupus, postinfectious, cryoglobulinemia, primary m
embranoproliferative glomerulonephritis)
Tubular
Ischemi
Totoxic
Heme pigment (rhabdomyolysis, intravascular hemolysis)
Crystals (tumor lysis syndrome, seizures, ethylene glycol poisoning, m
egadose vitamin C, acyclovir, indinavir, methotrexate)
Drugs (aminoglycosides, lithium, amphotericin B, pentamidine, cisplati
n, ifosfamide, radiocontrast agents)
Post-renal
Ureteric obstruction
Stone disease,
Tumor,
Fibrosis,
Ligation during pelvic surgery
Bladder neck obstruction
Benign prostatic hypertrophy [BPH]
Cancer of the prostate
Neurogenic bladder
Drugs(Tricyclic antidepressants, ganglion blockers,
Bladder tumor,
Stone disease, hemorrhage/clot)
Urethral obstruction (strictures, tumor)
Clinical feature-1
Signs
Clinical feature-2
Symptoms
weakness and
easy fatiguability (from anemia),
anorexia,
vomiting, mental status changes or
Seizures
edema
Systemic
fever
arthralgias,
pulmonary lesions
Diagnosis
Urinalysis
Unremarkable in pre and post renal causes
Differentiates ATN vs. AIN. vs. AGN
Muddy brown casts in ATN
WBC casts in AIN
RBC casts in AGN
Evaluation:
Treatment of
acute renal failure
Optimization
me status
Avoidance of further renal insults
Optimization of nutrition
If necessary, institution of renal replace
ment therapy
The function has to be temporarily
replaced by dialysis
of uremia ( encephalopat
hy,)
Uremic pericarditis
Refractory volume over load
Refractory hyperkalemia
Refractory metabolic acidosis
NEPHROLOGY
Prof univ dr Ion C Tintoiu
Definitions
Chronic Renal Failure
Results
unction
Occasionally results from rapid progression of
acute renal failure
Symptoms occur when 75% of function is lost b
ut considered cohrnic if 90-95% loss of function
Dialysis is necessary D/T accumulation or urem
ic toxins, which produce changes in major orga
ns
Subjective symptoms
Chronic Renal Failure
Subjective
te
Objective symptoms
Renal
Hyponaturmia
Dry mouth
Poor skin turgor
Confusion, salt overload, accumulation of K with
muscle weakness
Fluid overload and metabolic acidosis
Proteinuria, glycosuria
Urine = RBCs, WBCs, and casts
symptoms
Cardiovascular
Hypertension
Arrythmias
Pericardial effusion
CHF
Peripheral edema
Neurological
symptoms
GI
Stomatitis
Ulcers
Pancreatitis
Uremic fetor
Vomiting
consitpation
Respiratory
^ chance of infecti
on
Pulmonary edema
Pleural friction ru
b and effusion
Dyspnea
Kussmauls respir
ations from acidosi
s
symptoms
Endocrine
Hemopoietic
Anemia
Decrease in RBC surviva
l time
Blood loss from dialysis a
nd GI bleed
Platelet deficits
Bleeding and clotting dis
orders purpura and he
morrhage from body orif
ices , ecchymoses
symptoms
Skeletal
Skin
findings
Metabolic acidosis
Fluid imbalance
Insulin resistance
Anemia
Immunoligical problems
and insulin
Na bicarb, Ca, Vit D, phosphate binders
Fluid restriction, diuretics
Iron supplements, blood, erythropoietin
High carbs, low protein
Dialysis - After all other methods have failed
Vascular access
dialysis
Semipermeable membran
e
Catheter inserted through
abdominal wall into perito
neal cavity
Cost less
Fewer restrictions
Can be done at home
Risk of peritonitis
3 phases inflow, dwell an
d outflow
Automated peritoneal di
alysis
Done at home at night
Maybe 6-7 times /week
CAPD
Continous ambulatory pe
ritoneal dialysis
Done as outpatient
Usually 4 X/d
Transplant Meds
Patients
Cytotoxic
Imuran
Cytoxan
Cellcept
T-cell
depressors - Cyclosporin
NEPHROLOGY
Prof univ dr Ion C Tintoiu
. RENAL TUMOURS
CYSTIC DISEASES
. OF
THE KIDNEY
CYSTIC DISEASES OF
THE KIDNEY
Fluid
idney
May involve cortex or medulla or
both
May be unilateral or bilateral
May be unilocular or multilocula
r
May be congenital or acquired
May be sporadic or genetically d
CLASSIFICATIONS OF
RENAL CYSTIC DISEASES
Polycystic
kidney diseases:
1. Autosomal recessive (ARPKD)
classic infantile polycy
stic disease
with congenital hepat
ic fibrosis
2. Autosomal dominant (ADPKD)
Simple renal cysts
Acquired renal cystic disease
000 gms)
Diffuse cystic (1-2% cystic nephrons)
change with uninvolved intervening pa
renchyma
Varying sized, numerous to innumerabl
e generally spherical unilocular cyst
s, distributed in cortex and medulla
obscuring normal reniform shape and c
orticomedullary junction, containing
yellowish to turbid to brown to black
colored fluid
Distorted pelvi-calyceal system
Renal cancer
Renal cancer
In
NEPHROBLASTOMA ( Wilms
tumour )
Embryonal
NEPHROBLASTOMA
Clinical Features
Most
NEPHROBLASTOMA
prognosis and treatment
Depends
upon :
stage, age and histology
Surgery with chemotherapy for :
stage I & II with favorable his
tology
surgery with chemotherapy and r
adiotherapy for higher stages a
nd unfavorable histology
seems
triad :
hematuria, flank pain and abdom
inal mass
may be clinically occult, 30% pr
esents with metastatic lesion
Polycythemia due to erythropoiet
in
constitutional symptoms
imaging techniques - useful
prognosis
by multiple factors :
tumour size
infiltrative margins
histological type
tumour stage - most important
Can be expressed in terms of histol
ogical types
Incidental
findings at autopsy
(22%)
Well demarcated, unencapsulated
Pale yellow-gray, discrete cort
ical mass
Up to 2 cms. in maximum dimensi
on
Bladder Carcinoma
Derived
Present
Prognosis
Overall
5y survival = 50%
Nu s-a terminat !
. DIALYSIS
Dialysis
Definition
Artificial process that partially replaces renal f
unction
Removes waste products from blood by diffusi
on (toxin clearance)
Removes excess water by ultrafiltration (maint
enance of fluid balance)
Wastes and water pass into a special liquid di
alysis fluid or dialysate
Types
Haemodialysis
(HD)
Peritoneal Dialysis (PD)
They work on similar principles: Movement
of solute or water across a semipermeable
membrane (dialysis membrane)
Diffusion
Movement
of solute
Across semipermeable membrane
From region of high concentration to one of
low concentration
Ultrafiltration
Made
possible by osmosis
Movement of water
Across semipermeable membrane
From low osmolality to high osmolality
Osmolality number of osmotically active
particles in a unit (litre) of solvent
Haemodialysis
Dialysis
machine
The dialysis membrane is an artificial one: Dial
yser
The dialyser removes the excess fluid and wast
es from the blood and returns the filtered blood
to the body
Haemodialysis needs to be performed three tim
es a week
Each session lasts 3-6 hrs
AV Fistula Access
Matures
in about 6 weeks
Ensure good working order
Avoid tight clothing or wrist watch on fistula arm
Assess fistula daily; notify immediately if not working
Avoid BP cuff on fistula arm
Avoid blood sampling on fistula arm (except daily
D Rx)
Avoid sleeping on fistula arm
Grafts (synthetic) may be used to create an AV fistula
AV Fistula
AV Fistula
Hemodialysis
3-4
times a week
Takes 2-4 hours
Machine filters
blood and
returns it to
body
Problems with HD
Rapid changes in BP
fainting, vomiting, cramps, chest pain, irritability, fatigue, temporary los
s of vision
Fluid overload
esp in between sessions
Fluid restrictions
more stringent with HD than PD
Hyperkalaemia
esp in between sessions
Bleeding
from the fistula during or after dialysis
Infections
during sessions; exit site infections; blood-borne viruses e.g. Hepatitis, H
IV
is
Access is by PD catheter, a soft plastic tube
Catheter and dialysis fluid may be hidden unde
r clothing
Suitability
Excludes patients with prior peritoneal scarring e.g.
peritonitis, laparotomy
Excludes patients unable to care for self
Peritoneal Dialysis
.
contains:
buffer:
Lactate
e liver
Dextrose solution strengths: 1.5%, 2.5%, 4.25%
Types
Continuous Ambulatory
Peritoneal Dialysis
(CAPD)
Automated peritoneal Dialysis (APD)
Continuous cyclical
Intermittent
CONTROLLING DIET
Foods to control are those containing:
Protein
Potassium
Sodium
Phosphorous
Fluid
FLUIDS
Healthy
Check
Need
VITAMINS
Folic
Iron
Do
acid
supplements
MANAGING DIET
INDICATORS OF GOOD CONTROL:
Blood
pressure
Swelling
Blood
samples
Plasmapheresis:
plasma exchange and immunoadsorption
?
.
. Kidney Stones
ETIOLOGY
HYPEREXCRETION OF RELATIVELY INSOLUBLE URINARY
CONSTITUENTS
stone is relatively rare. Cabbage, rhubarb, spinach, tomatoes, black tea and cocoa
contain large amount of oxalate. Ingestion of excessive amounts of ascorbic acid
and orange juice also increase urinary oxalate excretion.
2. Calcium - On regular diets normal urinary excretion of calcium ranges
between 200 mg to 300 mg per day. The major calcium in foods are in milk and
cheese. Milk and dietary protein also cause increased absorption of calcium from
the gut.
3. Uric acid - Many patients with gout form uric acid calculi
particularly when under treatment. If the urine is made alkaline
and dilute while treating this disease chance of uric acid stone
formation is less
4. Cystine
Cystinuria is an herditary disease which is more common
in infants and children. Only a small percentage of patients with
Cystinuria form stones.
5. Drug induced stones
In rare cases, the long term use of magnesium trisilicate in
the treatment of peptic ulcer has produced radio opaque silicon
stones.
LOCATION OF STONES IN
KIDNEY
EFFECTS OF STONE
The size and position of the stone usually govern the development
of secondary pathologic changes in the urinary trace.
A. SAME KIDNEY
1. Obstruction
2.
Infection
B
OPPOSITE KIDNEY
1. Compensatory hypertrophy
2. Stone formation may be bilateral
3. Infection
4. Calculus anuria
CLINICAL FEATURES
Symptoms - Symptom wise cases can be divided into 4 groups :1. Quiescent calculus A few stones, particularly the phosphate
stones, may lie dormant for quite a long period.
These stone are also discovered due to symptoms of Urinary
Infection
2. Pain - Plain is the leading symptom of renal calculus in majority of
cases (80%). Three types of pain .
a) Fixed renal pain
b) Ureteric colic
c) Referred pain
3. Hydronephrosis
4. Occasionally haematuria is the leading and only
symptom.
(b)
(c)
3.Radiography
A) STRAIGHT X-RAY - Before taking straight X-ray for KUB region (both
kidneys, ureters and bladder), the bowels must be made empty by giving laxative.
B) Excretory Urogram
4 Ultrasonography
Helpful to distinguish between opaque and non-opaque stones. It is also of
value in locating the stones for treatment with extra corporeal shock wave therapy.
5 Computed topography
Particularly helpful in the diagnosis of non-opaque stones.
6 Renal Scan
7 Instrumental examination :- Cystoscopy
8
MANAGEMENT OF NEPHROLI
THIASIS
ASYMPTOMATIC CALCULI
TREATMENT
Solitary kidney
Occupation (pilot, business traveler
Simultaneous contralateral treatment
Its difficult to make an asymptomatic patient
feel any better !
STONE MANAGEMENT
OPTIONS
Open surgery
Percutaneous
nephrolithotomy
Ureteroscopy
Shock wave lithotripsy
Medical therapy
STONE MANAGEMENT
OPEN surgery NEPHROLITHOTOMY
STONE MANAGEMENT
PERCUTANEOUS NEPHROLITHOTOMY
SURGICAL STONE
MANAGEMENT
STAY OUT OF TROUBLE
Pre-op KUB
Pre-op IVP
URETERAL CALCULI
URETERAL CALCULI
TREATMENT OPTIONS
Observation
Shock wave lithotripsy
Ureteroscopy
Blind basket extraction
Percutaneous approach
Open surgery
?
.
. FINAL
Infection:
direct (BK virus, TBC, acute pyelonephritis),
indirect( Streptococci)
Immunologic
Allergic: drug induced
Auto-immune: Sjgren syndrome
Alloimmune: acute cellular allograft rejection
Unknown: IgG4- associated acute interstitial nephritis
Toxic: Pb poisoning, cadmium poisoning, Balkan endemic nephro
pathy
Metabolic: oxalosis secondary to malabsorbtion , gout
Obstruction: ureteral- pelvic junction stenosis:
Radiation: radiation interstitial nephritis
Idiopathic: sarcoidosis
rular diseases: 1%
d) idiopathic disease: 4%
Histology:
Early signs: oedema, lymphocytes focally
Later: eosinophils, lymphocytes, plasmocytes and histiocytes with
AcuteOedema
drug
induced interstitial
and focal inflammation
nephritis
Granuloma
EOS
Granuloma
0% in 1 to 12 mths
Irreversible with analg
esics, NSAIDs, longter
m use
Adverse
prognostic fe
atures
Marked interstitial infl
ammation
Granuloma (50% irrev
ersible)
Tubular atrophy
Fibrosis
s
In casu there is tubular destruction: histiocytes accumulate
Tubulitis with disappearance of the brush border in proximal tubul
es
Papillary sclerosis
CIN
Interstitium in transplants
Calcineurin inhibitors:
Heart, liver, pancreas, kidney transplants in diff
erent doses
Different levels of interstitial damage
Most structural nephrotoxic effects in arterioles
and glomeruli are manifestations of Thrombotic
MicroAngiopathy(TMA) with different patterns
of severity. The interstitial fibrosis has an uncer
tain pathogenesis but is probably vascular.
polyoma infection
In peritubular capillaries (PTC): lymphocytes+
+
Cellular rejection
Tubulitis
CD3
Acute pyelonephritis
Etiology:
Acute pyelonephritis
Chronic pyelonephritis
Etiology:
reflux
Histology:
- wedge shaped interstitial fibrosis(follows the
traject of the papillae and ascending tubules) acco
mpanied by tubular atrophy, vascular atheromatosi
s, glomerular sclerosis, inflammation
- outside the wedges: normal parenchyma but
with secondary changes in the glomeruli: glomerul
ar hypertrophy, FSGS
Chronic pyelonephritis
Chronic pyelonephritis
Tubular disease
Acute
tubular damage:
Myoglobinuria
Heavy metal exposure (Pb, Cd)
Oxalate crystal deposits: ethylene glycol toxicity
Calcineurin inhibitors: megamitochondria, isometric vacuolisat
ion
Tubular damage
URETERAL CALCULI
PARAMETERS FOR COMPARISON
Stone-free is not everything !!
URETERAL CALCULI
PARAMETERS FOR COMPARISON
Effectiveness
Morbidity
Convalescence
Cost
SWL FOR
URETERAL CALCULI
DORNIER HM-3
Upper Middle Lower
N= 33 N=248 N=381
Success of 94.8% 85.9% 98.2%
1O procedure
Re-tx rate 6.8% 15.7% 1.8%
Complications 10% 15.3% 8.4%
SWL OF DISTAL
URETERAL CALCULI
ADVERSE EFFECTS TO
FEMALE REPRODUCTIVE TRACT?
Initial animal studies suggest ovarian trauma Imp
aired fertility
Mutagenesis
Subsequent animal investigations demonstrate no im
pact on fertility or offspring
Mice
Rats Rabbits
SWL OF DISTAL
URETERAL CALCULI
ADVERSE EFFECTS TO
FEMALE REPRODUCTIVE TRACT?
URETEROSCOPY
URETERAL CALCULI
FLEXIBLE URETEROSCOPY
ANTEGRADE MANIPULATION OF
URETERAL CALCULI
INDICATIONS
Large stone burden
Body habitus
Urinary diversion
Transplant kidney
URETERAL CALCULI
PERCUTANEOUS APPROACH
NEPHROLITHIASIS
NATURAL HISTORY & RISK FACTORS
Peak incidence age 30 - 60
Gender (Male : Female) 3 : 1
Family history 3 - fold risk
Body size risk with weight
Recurrence after first stone:
Year 1 10 - 15%
Year 5 50 - 60%
Year 10 70 - 80%
One Year
Two
Post SWL
Post
8%
22%
3 Mo PostLithotripsy
Lithotripsy
254
261
552
548
249
257
42
41 Brown, et al, 1989
STONE FORMATION
MAJOR FORCES
Concentration / solubility of stone-forming sal
ts
Promoters of crystallization and aggregation
Inhibitors of crystallization and aggregation
DIETARY CALCIUM
IMPACT OF LOW CALCIUM DIET
Early recommendations suggest that low calcium diet
will decrease urinary Ca++ excretion, thereby reducing r
isk of stone formation
Potential risk factors involving low calcium diet:
Reduced bone mass
Increased urinary oxalate
DIETARY CALCIUM
RECOMMENDATIONS
Moderate calcium restriction in patients with A
H
Limit dietary intake of oxalate
Spinach, tea, chocolate, nuts
Limit dietary sodium intake
CALCIUM SUPPLEMENTS
PHYSIOLOGICAL EVIDENCE
Calciuric response to calcium supplementation
Depends on duration of treatment and patient popula
tion
CALCIUM SUPPLEMENTS
RECOMMENDATIONS:
PREMENOPAUSAL WOMEN
Give HCTZ during initial three months to prevent hyp
ercalciuria, then discontinue for one month
If urinary calcium up at 4 months, re-start HCTZ
Alternative: Significantly increase fluid intake for firs
t three months and then check 24-hour urinary calcium
Answer 1.
Renin Angiotensin II- ACE- ADH Aldosterone
That is not correct
Please try again
Peritoneal Dialysis
Is performed as an intracorp
oreal (inside the body) therap
y making use of the peritonea
l membrane.
Is the process of cleaning the
blood by using the lining of th
e peritoneal cavity (peritoneu
m) as a filter the peritoneu
m acts as a dialyzing membra
ne, permitting wastes from th
e body to cross it and empty i
nto the instilled dialysate flui
d.
Is a type of dialysis usually do
ne by the patient at home.
What do
the kidneys do??
Hemodialysis
3-4
times a week
Takes 2-4 hours
Machine filters
blood and
returns it to
body
Peritoneal Dialysis
Abdominal
3
types
Continuous ambulatory
Continuous cyclical
Intermittent
Questions?