1- Enlist electrolytes and nonelectrolytes particles in the body?
v Electrolytes – charged particles
§ Cations – positively charged ions ( Na+, K+ , Ca++, H+ ) § Anions – negatively charged ions ( Cl-, HCO3- , PO43- )
v Non-electrolytes – Uncharged ( Proteins, urea, glucose, O2, CO2)
1) Antidiuretic hormone.
2) Aldosteron hormone.
3) Natriuretic peptide hormone.
2- What are the Primary Regulatory Hormones Affecting fluid and
electrolyte balance?
3- Classify the Buffers system types?
1) 2) 3)
Indications for TPN Short-term use
.
Bicarbonate buffer system.
Phosphate buffer system
Protein buffer system.
4- What are the indications for total and partial parenteral therapy?
§ Bowel injury, surgery, major trauma or burns § Bowel disease (e.g. obstructions, fistulas)
§ Severe malnutrition
§ Nutritional preparation prior to surgery.
§ Malabsorption – bowel cancer
§ Severe pancreatitis
§ Malnourished patients who have high risk of § Aspiration
Long-term use (HOME PN)
§ Prolonged Intestinal Failure
§ Crohn’s Disease
§ Bowel resection
§ § §
5- Discuss the renal arterial blood supply?
Renal artery.
Accessory renal artery:
Renal vein : from the hilum into inferior vena cava
6- What are the different between Female Urethra and Male Urethra?
§
§ § § §
Male Urethra:
Divided into three portions, the prostatic, membranous, and cavernous/penile/spongy
Prostatic : widest and most dilatable part , 3 cm. long
The membranous portion: shortest, least dilatable
Spongy part: longest part of the urethra 15 cm. long
Female Urethra
§ 3to4cmlong
§ External urethral orifice between vaginal orifice and clitoris
§ Internal urethral sphincter detrusor muscle thickened, smooth
muscle, involuntary control
§ External urethral Sphincter :skeletal muscle, voluntary control
7- Describe the location and shape of kidney?
§ Are reddish brown, beans shaped.
§ Lie behind the peritoneum,
§ Extend from T12 to L3 vertebra.
§ The right kidney lies slightly lower than the left kidney because of
the large size of the right lobe of the liver.
8- Discuss the renin angiotensin work?
• Renin acts on angiotensinogen in the plasma, converting it to angiotensin I.
• Angiotensin I is converted by angiotensin-converting enzyme (ACE) to angiotensin II
• Angiotensin II
• A potent vasoconstrictor à increase blood pressure
• Stimulates release of aldosterone in the adrenal cortex.
Aldosterone stimulates the epithelial cells of the distal convoluted tubule to remove Na and Cl from lumen of tubules to the blood. Water follows the ions à increase the fluid volumeàincrease blood pressure.
9- What is counter current mechanism?
• A counter current mechanism is a system in which the inflow runs parallel to, counter to and in close proximity to the outflow.
10- What is the Mechanism of Micturition?
• Micturition is fundamentally a spinobulbospinal reflex facilitated and inhibited by higher brain centers like defecation, subject to voluntary facilitation and inhibition.
11- Summarize the steps of urine formation?
1- Glomerular filtration Creates a plasma like filtrate of the blood (i . 2- Tubular reabsorption Removes useful solutes( glucose, amino acid ,
water ) from the filtrate, returns them to the blood .
3- Tubular secretion Remove wastes ( H , K , cearatinin , drug ) from the peritubular blood and secreted them by the tubule cells into
filtrate .
4- Concentration Removes water from the urine, concentrates wastes.
12- What are the factors that Stimulate thirst center?
( hypothalamic thirst center )
1-
decline in plasma volume of 10%–15% . 2- increases in plasma osmolality of 1–2% . 3- baroreceptor input, angiotensin II .
13- What is mechanism of action of Hydrochlorothiazide? What are
adverse effects of furosemide?
v Mechanism of action:
– Inhibit active reabsorption of NaCl in (DCT) distal
convulated tubule by interfering with Na+ – Cl-
cotransporter (NCC), a specific Na+ -Cl- transport protein
v Adverse effects of furosemide :
• Hypokalemia & metabolic alkalosis
• ototoxicity (hearing loss)
• Hyperuricaemia
• Hypocalcemia & hypomagenesemia
• Hyponatremia, dehydration, hypovolemia • Hyperglycemia and hyperlipidemia
• GIT disturbances
• Allergic reactions
• • •
• •
step1. Ascending infection : most important route for kidney infection
¡AdhesionofentericbacteriaàColonization ofdistal Urethra à enhanced by specific adhesions molecules& fimbriae promote renal tropism à persistence of infection,.
Step2. From the urethra to the bladder: expansive growthàbladder o a. Urethral catheterization or other instrumentation.
o b. the shorter urethra in females.
o c. Urethral trauma during sexual intercourse.
Step3. The reflux allows bacteria to ascend the ureter into the pelvis
¡ In the presence of stasisàInfected bladder urine can be propelled up to the renal pelvis
¡ VUR [20% to 40% of young], acquired & congenital defect that results in incompetence of the uretero-vesical valve.
Step4. Intra-renal reflux:
¡ Further into the renal parenchyma through open ducts at the tips of the papillae.
15- The pathogenesis of Pyelonephritis?
The most common agent is E.coli
Routes of spread to the kidney: There are two routes by which bacteria
can reach the kidneys
1- Ascending infection- from the lower urinary tract [important route]
Urinary bladder infection.
Vesicoureteral reflux.
Intrarenal reflux.
2- Hematogenous infection-
less common
Seeding of the kidneys by bacteria in the course of septicemia or
infective endocarditis .
15- Differentiate between Nephritic Syndrome and Nephrotic
Syndrome?
• It is a clinical complex usually of
Nephrotic syndrome refers to clinical condition
cell casts.
acute onset
• characterized by five criteria:
1. Hematuria with diagnostic red
2. Oliguria and impairment of
kidney function.
3. Hypertension
. 1. Mild proteinuria.
• five main features;
• Massive proteinuria (more than 3.5
gm/day)
• Hypo-albuminaemia (less than 3
gm/dl)
• Generalized edema
• Hyper-lipidaemia (increase
cholesterol & triglycerides)
• Lipiduria (Lipid casts in urine ).
2. Mild edema (localized to face)
Pathogenesis
Pathogenesis
• The initial event is damage to
capillary wall
• resulting in increase permeability to
plasma protein.
• With long standing heavy proteinuria
serum albumin tend to become
depleted and decreased.
• The drop of osmotic pressure will lead
to generalized edema .
• As fluid escape from vessels to tissues,
1. there is decrease of plasma
volume with
2. compensatory secretion of
aldosterone
3. resulting in salt and water
retention and
4. further aggravate the edema. • Hypo-albuminaemia trigger
increased synthesis of lipids in the liver.
• GFR is decreased due to obstruction
of glomerular lumen by
• The proliferating glomerular cells
• Infiltrating inflammatory cells
• Due to haemodynamic changes
(vasoconstriction) .
• The inflammatory reactions injure the
capillary wall and produce
hematuria.
• Reduced GFR is manifested clinically
by oliguria .
• Hypertension is the result of both
• Fluid retention and
Renin release from ischemic kidney
• Primary
– Postinfectious / Diffuse proliferative
GN
– Membranoproliferative GN
– IgA nephropathy
(Mesangioproliferative GN)
– Crescentic GN
• Secondary
– HSP
– Systemic vasculitis
– SLE
– Systemic sclerosis
Primary Glomerular Disease Membranous glomerulonephritis (GN) Lipoid nephrosis mal change disease) Focal segmental glomerulosclerosis GN Membranoproliferative Proliferative GN (foca “pure mesangial. IgA nephropathy)
Systemic Disease Diabetes mellitus Amyloidosis Systemic lupus erythematosus Drugs (gold, penicillamine, street heroin”) Infections (malaria, syphilis. hepatitis B AIDS) Malignancy (carcinoma, melanoma) Miscellaneous (bee-sting allergy, hereditary nephritis)
16-Discuss the role of kidneys in regulation of acid base balance
REABSORPTION OF BICARBONATE
Conservation of bicarbonate – proximal tubular cells
Na+ – H+ antiport system
~Urine is free of HCO3-
~Simultaneous excretion of H+, prevents loss of sodium
NEW BICARBONATE GENERATION
Elimination of nonvolatile acid
~Excretion of H+
~Occurs in DCT and collecting ducts
~Generation of bicarbonate
~H+ combine with non carbonate base and excreted
Urinary buffers
hydrogen ion excretion requires – presence of suitable buffer system in
urine
Minimum pH of urine – 4.5
~role of phosphate buffer – pK’ – 6.8
Most important buffer
EXCRETION OF AMMONIUM ION
NH3 is obtained from deamination of glutamine
NH4+ cant diffuse back
2/3 of body acid load liberated in the form of NH4+
17-List factors the affect GFR
1. Age : GFR decreases with increasing age
2. Renal blood flow: is directly proportional to GFR
3. Hydrostatic pressure in glomerular capillary (PG ):
i. ii.
4. 5. 6. 7.
8.
Systemic blood pressure- is proportional to GFR when BP below or above this range ( 90mm Hg – 220mm Hg ) .
– Between this range GFR is stabilized by renal
autoregulation.
Afferent and efferent arteriolar constriction-
–
constriction of afferent arteriole : reduces both renal plasma flow and GFR.
a moderate constriction of efferent :slight increase in GFR
–
–
Hydrostaticpressureinthebowman’scapsule(PB) Changesinconcentrationofplasmaprotein(πG) Stateofglomerular(filtering)membrane Sizeofcapillarybed:contractionofmesangialcells:decreases GFR.
Pregnancy
severe constriction : decrease in GFR.
18-what are the constituents of Juxtaglomerular apparatus
-macula densa
– extraglumerular mesangial cells
– juxtaglomerular (granular cells) cells
19- Define anion gap
The difference between measured cations (Na + K) and anions (Cl + HCO3)
20- Describe the clinical manifestations of acid-base disorders
v Acidosis :
• depression of the CNS through ↓ in synaptic transmission.
• Generalized weakness
• Deranged CNS function is the greatest threat
• Severe acidosis causes
o Disorientation o Coma
o Death
vAlkalosis :
• • • •
over excitability of the central and peripheral nervous systems. Numbness
Lightheadedness
Severe Alkalosis cause :
o Nervousness
o muscle spasms or tetany o Convulsions
o Loss of consciousness
o Death
21- Development of urinary system
MCQ
Controls colloidal osmotic pressure. Albumin
Globulin
Fibrinogen
Acute tubular necrosis (ATN) common cause
acute renal failure.
the psoas muscle
common iliac artery ischial spine
Relations – Right Kidney Anterior: Liver
Spleen
Stomach
Pancreas
Visceral layer of Bowman’s capsule: simple squamous epithelium special epithelium (podocytes)
Separated by from the tips of the transverse processes of the lumbar
vertebrae.