S.Y.B.

Pharm:
PHT1208 Anatomy, Physiology & Pathology-II
  Course contents (Topics and subtopics)
1 Nervous System/sense organs. Anatomy-Physiology of CNS (Central N.S)
2 Anatomy-Physiology of PNS (Peripheral NS) and ANS (Autonomic NS)
3 Neurotransmitters, Neurotransmission, Sensory- Motor pathways; Cranial – Spinal Nervous; Blood –Brain Barrier,
Blood flow to brain
4 Diseases – Parkinsonism, Alzheimer’s and epilepsy
5 Sense organs: Anatomy and Physiology; Physiology of sensations (special)
6 Digestive System|: Anatomy-Physiology including liver, pancreas. Diseases: Peptic Ulcers, hepatitis
7 Cardiovascular System: Anatomy – Physiology,Structure and conducting systems of heart. Generation of action
potential in SA node and itsconduction/ Action potential in cardiac muscle. Cardiac cycle,ECG, (P-QRS-T)
8 Blood pressure-factors modifying blood pressure
Baroreceptors, Chemoreceptors, Vasomotor centre, humoral and neuronal regulation of Blood pressure and
Circulation
9 Diseases: Hypertension, CCF, Arrhythmia, angina pectoris, IHD, arteriosclerosis.
10 Urinary System: Anatomy – Physiology
Function of kidneys and formation of urine. Maintainence of acid- base and electrolyte balance, Renin-angiotensin
system.
11 Urine analysis- Volume, colour, odour, specific gravity, normal and abnormal constituents with associated diseases.

List of Text Books/Reference Books

Anne Waugh and Allison Grant, Ross and Wilson’s Anatomy and Physiology in Health and Illness , 12th edition, Churchill Livingstone, London, 2014
Gerald J. Tortora and Sandra, Principles of Anatomy and Physiology, 14th edition, John Wiley and Sons Inc, New York, USA, 2014
Arthur C. Guyton and John E. Hall, Textbook of Medical Physiology, 13th edition, 2016, W.B.Saunders Company, Pensylvania, U.S.A, 2016
B. R. Mackenna and R. Callander, Illustrated Physiology 6th edition, , Churchill Livingstone, New York, London, 1997 1

Anne Waugh and Allison Grant, Ross and Wilson’s Anatomy and Physiology in Health and Illness , 12th edition, Churchill Livingstone, London, 2014
 Urinary System
S.Y. B. Pharm: Pharmacology II
Dr. Vaibhavi Peshattiwar
Institute of Chemical Technology

2
URINARY SYSTEM
 Kidneys

 Paired
 Reddish, kidney bean shaped.
 Located just above the waist between
peritoneum and posterior wall of abdomen.
 Located between last thoracic and L3
 Partially protected by 11th and 12th ribs.
 Right kidney slightly lower than left .

Adult Kidney
• Length: 10-12 cm (4–5 in.)
• Width: 5-7 cm (2–3 in.)
• Thickness: 3 cm (1 in.)
• Mass of 135–150 g (4.5–5 oz)
External Anatomy of the Kidneys
 Layers of kidneys:
1. Renal capsule
2. Adipose capsule
3. Renal fascia

Blood supply to kidneys:

• Kidneys constitute less than 0.5% of body mass
• Receive 20- 25 % of total cardiac output via renal arteries.
• In adults, renal blood flow (blood flow through both kidneys)= 1200ml/min
 Internal anatomy of kidneys

Minor calyx

Major calyx
 FUNCTIONS OF KIDNEY
1. Excretion of wastes and foreign substances:
• Wastes resulting from metabolic reactions s.a. ammonia and urea from deamination of
amino acids, bilirubin from catabolism of hemoglobin etc.
• Foreign substances from diet and xenobiotics and their metabolites

2. Regulation of
a. Blood volume: conserving or eliminating water in urine. Increase in blood volume
increases b.p. and vice versa.

b. Blood Pressure: Release of renin and activating renin-angiotensin- aldosterone

pathway.

c. Ionic composition: Blood level of several ions s.a. Na+, K+, Cl-, Ca2+, HPO42-

d. pH: Regulating the excretion of H+ and bicarbonate ions (HCO3-)

• Maintaining acid-base balance.

e. Osmolarity: Controlling the loss of water and solutes.

• Approx. 300 mOsm/ liter
3. Production of hormones

a. Calcitriol: Active form of Vit. D, regulate calcium homeostasis.

b. Erythropoietin: Stimulate RBC production.

 STRUCTURE OF A NEPHRON
Renal Corpuscle

Descending limb of
loop of hele

Ascending limb of
loop of henle
Renal Corpuscle
Filtration membrane
I. The endothelial cells  of the glomerulus :
• Contain numerous pores (fenestrae) that, unlike those of other fenestrated capillaries,
are not spanned by diaphragms.
• The cells have fenestrations that are 70 to 100 nm in diameter.
• Permits filtration of all solutes but prevents blood cells and platelets.

II. Basal lamina:

• Layer of acellular material between endothelium and the podocytes.
• Prevents filtration of larger proteins.

III. Slit membrane between pedicles:

• Thin membrane which extends across the spaces between the pedicles (filtration slits).
• Permits passage of molecules smaller than 6-7nm.
• Include water, glucose, vitamins, amino acids, very small plasma proteins, ammonia,
urea and ions.
• Prevents passage of albumin (diameter 7.1 nm).
Histological Features of the Renal Tubule and Collecting Duct
 Renal Physiology: Process of urine formation
1. Glomerular flitration: 1st step, water and solutes move
across the wall of glomerular capillaries into glomerular
capsule.
2. Tubular reabsorption: Tubule cells reabsorb about 99% of
filtered water and useful solutes. Reabsorbed substances
return to the blood as it flows through the peritubular
capillaries and vasa recta.
3. Tubular secretion: Tubule and duct secrete materials such as
wates, drugs and excess ions into the tubular fluid
4. Metabolism:In this phase urine is acidified due to secretion
of H+ ions.
For any substance S,

Excretion rate of S = (Rate of glomerular filtration of S + Rate of secretion of S)

- Reabsorption rate of S.
 Glomerular filtration: NET FILTRATION PRESSURE
Glomerular filtration depends upon 3 main pressures:
1. Glomerular blood hydrostatic pressure (GBHP): + ve pressure.
Blood pressure in the glomerular capillaries. Promotes filtration by forcing water and solutes
through filtration membrane.
2. Capsular hydrostatic pressure (CHP): - ve pressure, Hydrostatic pressure excerted by fluid
already in the capsular space and renal tubule.
3. Blood colloid osmotic pressure (BCOP): - ve pressure, Pressure of proteins s.a. albumins,
globulins and fibrinogen in the blood plasma.

 Pressure of only 10 mmHg causes a normal amount of blood plasma to filter from the
glomerulus into the capsular space.
 Glomerular Filtration Rate

Glomerular filtrate: The fluid that enters the capsular space (protein free
plasma).
• Amount of filtrate formed in all the renal corpuscles of both the kidneys each
minute is the glomerular filtration rate.

• In adults average GFR is approx. 125 mL/min in males and 105 mL/min in
females.
• Approx. 180 L /day
• Urine output is about 1- 2 L /day
• About 99% of filtrate is reabsorbed.
Tubular Reabsorption and Secretion
Reabsorption Routes
Tubular Reabsorption and Secretion
By end of proximal tubule have reabsorbed:
• 60- 70% of water and sodium
• About 100% of organic solutes such as
glucose and amino acids
• 50% of the filtered Cl-, filtered urea.
• 90 % of K+, bicarb, Ca++, uric acid
• Secrete a variable amount of H+ ions,
ammonium ions (NH4+), and urea.
• Transport maximum – maximum amount of a
substance that can be absorbed per unit time
• Renal threshold – plasma conc. of a substance
at which it exceeds Tm.
 Loop of Henle

• Reabsorbs about 15% of the filtered water, 20–30% of the filtered Na+ and K+,
35% of the filtered Cl-, 10–20% of the filtered HCO3-, and a variable amount
of the filtered Ca2+ and Mg2+.

• Thin Descending limb has high permeability to water and low

permeability to ions: About 15% of the filtered water is reabsorbed in the
descending limb of the loop of Henle

• Thick ascending loop absorbs Na+, K+, Cl- by active transport by NKCC2

• Electrical and concentration gradient drives more resorption of cations like

Ca++ and Mg++ along with Na+

• Little or no water is reabsorbed in the ascending limb.

• The osmolarity of the tubular fluid decreases progressively as fluid flows

toward the end of the ascending limb.

• Cortical thick limb drains into distal convolute tubule

 DISTAL CONVOLUTED TUBULE AND COLLECTING
DUCTS

Early DCT
• The early or initial part of DCT reabsorbs about 10–15% of the filtered water,
5% of the filtered Na+, and 5% of the filtered Cl-.
• Reabsorption of Na+ and Cl- occurs by means of Na+ – Cl- symporters in the
apical membranes.
• Major site for parathyroid hormone (PTH) stimulated calcium (Ca2+)
reabsorption
• The amount of Ca2+ reabsorption in the early DCT varies depending on the
body’s needs.
• Tubular secretion to rid body of substances: K+, H+, urea, ammonia,
creatinine and certain drugs
• Secretion of H+ helps maintain blood pH
(can also reabsorb bicarb and generate new bicarb)
Late Distal Convoluted Tubule and Collecting Duct

• The principal cells reabsorb Na+ and secrete K+; the intercalated cells
reabsorb K+ and HCO3- and secrete H+.

• Na+ leakage channels rather than by means of symporters or antiporters

• The mechanism employed for K+ excretion is the major source of its

excretion in urine.
 Hormonal Regulation of
Tubular Reabsorption and Tubular Secretion
Antidiuretic Hormone
PRODUCTION OF CONCENTRATED AND DILUTE URINE
Mechanism of urine concentration in long-loop juxtamedullary nephrons.
 Production of Dilute Urine

Formation of dilute urine:

• ADH level is very low.
• Mostly cortical nephrons involved.
• Concentration of urine can be 65- 70 mOsm/L
• Four times more dilute than blood plasma or glomerular filtrate.
• PCT isotonic fluid as both ions and water absorbed
• urea, water,K+,Na+,Cl-, glucose, amino acids, lactate,Po4-3, and HCO3-
• Loop receives 1/3 of of original filtrate due to water absorption, and isotonic fluid
• 1200 mOsm/L is molarity in interstitium of inner medulla (600 mOsm/L in outer)
• Water diffuses in descending portion of loop of Henle as loop osmolarity is 300
mOsm/L
• Collecting duct reaches this highest concentration with maximum ADH effect
• Ascending loop receives still lower volume and different characteristic fluid
• This part impermeable to water but resorb solutes via Na-K-2Cl symporter and
Na-H antiporter till it reaches  100-150 mOsm/L(hypotonic)
• Called the diluting segment of nephron
• The loop capillaries ‘vasa recta’ has low flow which is important or else kidneys
will loose its ability to concentrate.
• Hydrogen antiporter is from Carbonic anhydrase forming H+ and HCO3-
• This maintains pH of the blood.
 Urine Analysis
Characteristics Description
Volume 1-2 L in 24 hrs
Color Yellow or amber but varies with urine concentration and
diet.
Color due to
Urochrome (pigment produced from breakdown of bile)
Urobilin (from breakdown of hemoglobin)
Diet , medication and certain drugs affect color.
Turbidity Transparent when freshly
Becomes turbid (cloudy) on standing
Odor Midly aromatic but becomes ammonia like upon
standing.
pH 4.6- 8, Avg- 6
High protein diet: increases acidity
Vegetarian diet: increases alkalinity
Specific gravity 1.003-1.035
 NORMAL URINE VALUES

VOLUME 1-1.5 L
pH 5-7
Sp.gravity 1.002-1.030
Urine Bilirubin Negative
Urine Blood Negative
Urine ketone Negative
Leucocytes Negative
RBCs: 0-2/ HPF
WBCs:0-2 /HPF
RBC casts: 0/HPF
Nitrite Negative
Protein Negative-Trace

Urobilinogen 0.2-1.0 EhrU/dL

 Abnormal constituents in urine

Constituents Condition and diseases

Albumin Albuminuria, indicates an increase in the permeability of the
filtration membrane due to injury or disease, irritation due to
bacterial toxins heavy metals etc, high B.P.

Glucose Glucosuria, Diabetes mellitus

RBC Hematuria, Inflammation, irritation from kidney stones, tumors,
glomerulonephritis.

Ketone bodies Ketonuria, Diabetes mellitus, starvation

Bilirubin Bilirubinanuria, liver disease
Urobilinogen Urobilinogenuria, anemia, hepatitis, biliary obstruction, jaundice
Microbes Vary with the infection in the UTI, E.coli, C. albicans (Vaginitis)
Pus cells Infections
Crystals Crystals of Ca oxalate, uric acid, Kidney stones
 Electrolytes in body fluids

1. Sodium (Na+):
• Most abundant ion in the extracellular fluid, ≈ 90% of extracellular cation.
• Normal blood plasma conc= 136- 148 mEq/liter
• Pivotal role in fluid and electrolyte balance because it accounts for almost
half of the osmolarity of the extracellular fluid (142 of about 300 mOsm/L)
• Deficiency: Hyponatremia
• Excess: Hypernatremia.

2. Chloride:
• Most abundant anion in ECF.
• Normal blood plasma conc= 95- 105 mEq/liter
• Balance the levels of anions in different fluid compartments
• Deficiency: Hypochloremia
• Excess: Hyperchloremia.
3. Potassium:
• Most abundant cation in intracellular fluid
• Normal intracellular conc= 140 mEq/liter
• Normal blood plasma conc= 3.5-5 mEq/liter
• Important role in action potential: repolarization and maintenance of resting
membrane potential in neurons and muscles.
• Maintenance of normal intracellular fluid volume.
• Regulation of pH of body fluids: Exchanged for H+ during movement in or
out of cell.
• Deficiency: Hypokalemia; excess: Hyperkalemia

4. Bicarbonate (HCO3-):
• Second most prevalent extracellular anion
• Normal blood plasma HCO3- conc is 22-27 mEq/L
• Important role in acid- base balance and anion concentration in
extracellular and intracellular fluids.
5. Calcium:
• About 98% present in bone and teeth.
• Mainly an extracellular cation.
• Normal plasma conc. is 4.5- 5.5 mEq/L, same conc. is attached to various
plasma proteins.
• Hardness of bones and teeth, blood clotting, muscle tone, excitability of nervous
and muscle tissues.
• Deficiency leads to hypocalcemia whereas hypercalcemia is due to excess of
calcium in blood.

6. Phosphate ions (HPO42-):

• Intracellular anion ≈ 100 mEq/L
• Normal plasma conc. is 1.7- 2.6 mEq/L
• Important buffer of H+ in body fluids and urine

7. Magnesium:
• Second most common intracellular cation ≈ 35 mEq/L
• Normal plasma conc. is 1.3- 2.1 mEq/L
• Co-factor for certain enzymes involved in carbohydrate metabolism and sodium-
potassium pump
 Acid Base Balance

Critical importance for normal cellular functions.

Maintenance of acid base balance:

1. Buffer system of the body:
• The chemical compounds which converts strong acid or base into weak ones.
• Raise pH without removing H+

2. Respiration: Exhalation of CO2

• Change in the rate and depth of breathing can alter the pH of body fluids.
• H+ ions can be eliminated in form of carbonic acid by exhaling CO2.
• Doubling the ventilation can increase the pH from 7.4 to 7.63
• Decrease in ventilation can lower pH from 7.4 to 7
• Manipulation by respiration, within minutes

3. Excretion of H+ from urine

• Excretion of H+ by means of antiporters and proton pump.
• Only way to eliminate acids other than carbonic acid
• Slowest mechanism
 Buffers of Human Body

• Meaning of the word is to lessen or moderate the impact of something

• A buffer is a molecule that tends to either bind or release hydrogen ions in order
to maintain a particular pH.

• Buffers prevent rapid and drastic changes in the pH of body fluids by converting
strong acid and bases into weak acids and bases within fraction of seconds.
 
Three important buffer systems in our bodies:

1. Bicarbonate buffer system

2. Phosphate buffer system

3. Protein buffer system

 Carbonic acid- Bicarbonate Buffer System

Carbonic acid Bicarbonate ions

(weak acid) (weak base)

Excess of hydrogen ions (acidemia), some of those hydrogen ions will associate with
bicarbonate, forming carbonic acid, resulting in a smaller net increase of acidity than otherwise.
H+ + HCO3- H2CO3 H2O + CO2
Shortage of H+ or strong base, 
H2CO3 H+ + HCO3-

H2CO3 + NaOH NaHCO3 +H2O

• At pH 7.4, HCO3- = 24 mEq/L and H2CO3 = 1.2 mmol/L

• Concentration of bicarbonate buffering system can be regulated by kidney and respiratory
system.
 Phosphate Buffer System

Phosphoric acid Dihydrogen Monohydrogen

Phosphate Phosphate
(weak acid) (weak base)
• Nucleic acid and phosphoprotein break down yields phosphoric acid.  Phosphoric acid is H3PO4

• Phosphoric acid changes quickly into dihydrogen phosphate, or H2PO4-.   This dihydrogen
phosphate is an excellent buffer, since it can either grab up a hydrogen ion and reform phosphoric
acid, or it can give off another hydrogen ion and become monohydrogen phosphate, or HPO42-.
OH- + H2PO4 H2O + HPO42-
• Monohydrogen phosphate acts as a weak base, buffering H+ released from strong acids.
H+ + HPO42- H2PO4-
• In extremely basic conditions, monohydrogen phosphate can even give up its remaining
hydrogen ion.
• Therefore, the phosphate buffer system can accept or donate hydrogen ions depending on the
solution it is in.
• Important regulator of pH in the cytosol, since phosphates are major anions in intracellular
fluids
• Acts to a smaller degree in ECF and buffer acids in urine.
 Protein Buffer System
• Most abundant buffer in intracellular fluid and blood plasma.

• Proteins are made up of amino acids.

Amino acids have a central carbon with four groups
i.  a carboxyl group (COOH)
ii. an amino group (NH2)
iii. a hydrogen atom
iv. an R group

• When bicarbonate ions form, the hydrogen ions that are also products of bicarbonate
production are absorbed by the blood proteins.
• CSF is unable to do this efficiently as it has fewer proteins.

• At a near neutral pH, like the pH of blood, the carboxyl group is actually COO- instead of
COOH. 
• Then, if a protein finds itself in a more acidic solution, the carboxyl group will be able to take
on the extra hydrogen ions and return to the COOH configuration.
 The amino groups within protein amino acids are NH3+ even at neutral pHs.  But when they get
into basic pH solutions, they return to NH2.

 Amino acids can accept or donate hydrogen ions, making them excellent buffers. Any given
protein typically has hundreds of amino acids. 
 Respiratory Acidosis
A medical condition in which decreased ventilation (hypoventilation) causes increased
blood carbon dioxide concentration and decreased  pH (acidosis).

Two Types:
a) Acute: Occurs due to an abrupt failure of ventilation.

b) Chronic: occurs over a long period of time, may be secondary to many disorders,
including COPD.
Signs and Symptoms:
Headache Sleepiness
Tremors Anxiety
Delirium Blurred vision
Coma Restlessness
Causes: Chronic and Acute
• Asthma
• Chronic obstructive pulmonary disease (COPD)
• Severe obesity (which can interfere with expansion of the lungs)
• Neuromuscular disorders (such as multiple sclerosis that causes muscular weakness)
• Obstructed airways (due to choking or other causes)
• Sedative overdose: suppress breathing
• Cardiac arrest
 Diagnosis

1. Blood Gas Measurement: This test measures oxygen and CO2 in the blood. High
levels of CO2 can indicate acidosis.
2. Lung Function Tests: Many people with this condition have reduced lung function.
3. Chest X-Ray: X-rays can help doctors see injuries or other problems likely to cause
acidosis.
Treatment:
Acute Form
• Addressing the underlying cause. For example, your airway may need to be cleared as
soon as possible.
• Artificial ventilation may also be needed. 
Chronic Form
• Treatment focuses on managing underlying conditions with goal to improve airway
function.

• Some strategies include using:

i. Bronchodilators (To Expand The Airways)
ii. Mechanical Ventilation (in severe cases, to increase exhalation)
iii. Antibiotics (To Treat Infection)
iv. Diuretics (To Reduce Pressure On The Heart And Lungs)
v. Corticosteroids (To Reduce Inflammation)
 Respiratory Alkalosis
• A medical condition in which increased ventilation (hyperventilation) causes decreased
blood carbon dioxide concentration and increased  pH (alkalosis).
• This condition is basically the opposite of respiratory acidosis, when the blood becomes too
acidic.

Causes:
Hyperventilation increase occurs most often as a physiologic response to hypoxia, metabolic
acidosis, and increased metabolic demands (eg, fever: stimulates the respiratory centre in the
brainstem).
Hyperventilation without physiological need;
• Pain
• Anxiety
• Heart attack
• Higher altitudes
• Pulmonary diseases: such as pneumonia, where a hypoxic drive governs breathing more than
CO2 levels
• CNS disorders:  stroke
• Drug use: caffeine and coffee abuse
• Pregnancy
• Patients on mechanical ventilation
 Symptoms of Respiratory Alkalosis
• Dizziness
• Bloating
• Feeling light-headed
• Numbness and/or muscle spasms in the extremities (hands and feet)
• Discomfort in the chest area
• Confusion
• Dry mouth
• Tingling in the arms
• Heart palpitations
• Feeling short of breath
• Finally, an affected person may have a seizure in the most severe cases.

Diagnosis

1. Blood Gas Measurement: This test measures oxygen and CO2 in the blood. High levels
of CO2 can indicate acidosis.
2. Lung Function Tests: Many people with this condition have reduced lung function.
3. Chest X-Ray: X-rays can help doctors see injuries or other problems likely to cause
acidosis.
 Treatment for Respiratory Alkalosis

i. Treatment of the underlying cause.

ii. Breathe into a paper bag: Inhaling and exhaling into a paper bag for a short period,
thus inhaling air containing higher than normal conc. of CO2. A mask can also be used in
place of a paper bag.
iii. Restrict oxygen intake into the lungs. Some possible ways to do this are breathing
while pursing the lips or breathing through one nostril. For the second approach to be
useful, the mouth and the other nostril need to be covered.
 Metabolic Acidosis
Metabolic acidosis starts in the kidneys. It occurs when they can’t eliminate enough acid or when
they get rid of too much base.
• In metabolic acidosis, systemic arterial blood HCO3- level drops below normal

There are three major forms of metabolic acidosis:

1. Diabetic acidosis: Poorly managed diabetes. Ketones build up in the body and acidify the
blood (Ketosis).

2. Hyperchloremic acidosis: Loss of sodium bicarbonate. This base helps to keep the blood
neutral. Both diarrhea and vomiting can cause this type of acidosis.

3. Lactic acidosis : Excess of lactic acid in your body. Buildup of lactic acid can be due to
chronic alcohol use, heart failure, cancer, seizures, liver failure, prolonged lack of oxygen,
and low blood sugar, prolonged exercise.

4. Other factors that can contribute to your risk of metabolic acidosis include:
High-fat, low-carbohydrate diet
Kidney failure: Failure to excrete metabolic acids
Dehydration
Aspirin or methanol poisoning (Toxins metabolized to acids, formic acid for methanol)
 Symptoms(Metabolic acidosis)

• Rapid and shallow breathing

• Confusion
• Fatigue
• Headache
• Sleepiness
• Lack of appetite
• Breath that smells fruity – this is a sign of diabetic acidosis/ketoacidosis

Diagnosis

• Blood Gas Measurement

An arterial blood gas levels of oxygen and carbon dioxide in the blood. It reveals blood pH.
• Kidney function tests
• Measure of calcium, protein, blood sugar, and electrolyte levels.
 Treatment

• Hyperventilation: Less severe cases

• Hyperchloremic acidosis : Oral sodium bicarbonate.
• Diabetics with ketoacidosis receive IV fluids and insulin to balance out their pH.
• Lactic acidosis treatment might include bicarbonate supplements, IV fluids, oxygen, or,
antibiotics, depending on the cause.

Prevention
To Reduce The Risk of Metabolic Acidosis:
• Stay hydrated. Drink plenty of water and other fluids.
• Control of diabetes to avoid ketoacidosis.
• Alcohol prevention. Chronic drinking can increase lactic acid buildup.

Prognosis
• Quick, correct treatment has a strong influence on recovery. Sometimes complete recovery
and severe acidosis can cause shock or even death.
 Metabolic Alkalosis
Metabolic alkalosis develops when your body loses too much acid or gains too much base.
•In metabolic alkalosis, systemic arterial blood HCO3- level rises above normal

Causes:
1. Loss of excess acid: Excessive vomiting of gastric contents without voniting of lower GI
contents cause excessive loss of HCl.
2. Diuretics: Increased fluid flow in tubules leads to excess delivery of Na+ in DCT and CT.
Rapid reabsorption of Na+ causes enhanced excretion of H+ in urine.
3. Excessive intake of alkaline drugs: s.s Antacids for acidity and peptic ulcers.
4. Endocrine disorders: Aldosterone promotes enhanced reabsorption of Na+.

Symptoms
• Nausea
• Numbness
• Prolonged muscle spasms
• Muscle twitching
• Hand tremor
• if it isn’t treated right away, severe symptoms can develop
 Severe symptoms include
• Dizziness
• Difficulty Breathing
• Confusion
• Stupor
• Coma
Diagnosis
Urine analysis, Urine pH, Basic metabolic panel, and Arterial blood gas analysis.

Treatment
1. Treatment of the underlying cause.
2. Alkalosis derived from a chemical loss (such as chloride or potassium): medications or
supplements to replace these chemicals.
3. Tratment of electrolyte imbalance, which may be corrected by drinking plenty of fluids or
electrolyte-enhanced drinks.
4. Maintaining good health, eating a healthy diet, and staying hydrated.
 Glomerulonephritis

Renal disease due to inflammation of glomeruli

• Common most renal disease due to impairment of immune mechanism.
• Responsible for 50% of end stage renal failure.

Classification: Acute and chronic

• Acute glomerulonephritis: Develops over a short period of time, due to a sudden attack of
inflammation.
Most often occurs as a complication of a throat or skin infection with streptococcus, a type
of bacteria.

• Chronic glomerulonephritis: Progresses slowly.

Etiology:
Primary: Origin of inflammation within kidney.
Secondary: Systemic disease
Glomerulonephritis can be caused by various disorders, such as infections, an inherited
genetic disorder, or autoimmune disorders.
Acute glomerulonephritis:
• Postinfectious glomerulonephritis: occurs as a complication of a throat or skin infection
• Poststreptococcal glomerulonephritis: streptococci
• Infections with other types of bacteria, such as staphylococcus and pneumococcus, viral
infections, such as chickenpox, and parasitic infections, such as malaria.
• Noninfectious disorders: Vasculitis (blood vessel inflammation), Systemic lupus
erythematosus (lupus)

Chronic glomerulonephritis:
• Untreated acute form can progress in chronic form
• Genetic disease: Hereditary nephritis
• Unidentified cause.

Pathophysiology:
• Immunologic mechanism triggers inflammation and
proliferation of glomerular tissue that can result in damage
to the basement membrane and capillary endothelium.
• Proliferation of parietal epithelial cells leads to
the formation of crescents.
• Glomerular basement membrane thickening appears as
thickening of capillary walls on light microscopy.
• These structural changes can be focal, diffuse or segmental, or global.
 Inflammation leads to glomerular swelling and increase in permeability permiting filtration
of various solutes

Signs and symptoms:

Acute glomerulonephritis:
• Tissue swelling (edema): due to fluid retention, puffiness of the face and eyelids but later is
prominent in the legs
• Low urine volume,
• Hematuria: Presence of erythrocytes
• Variable degrees of proteinuria
• Blood pressure: Impaired kidney function.
Chronic glomerulonephritis:
• Hematuria, proteinuria (frothy urine)
• Hyperlipidemia: High blood levels of cholesterol, phospholipids, triglycerides
• Hypoalbuminemia: Low blood albumin levels
• High blood pressure (hypertension)
• Fluid retention (edema) with swelling evident in your face, hands, feet and abdomen
• Anemia
Diagnosis:
1. Urinalysis: protein and blood cells (RBC, WBC: infection), specific gravity.
CG : Urine random (spot) protein/creatinine ratio ≥ 3 or proteinuria ≥ 3 g/24 h.
2. Blood tests: Anemia abnormal albumin levels, abnormal blood urea nitrogen, and high
creatinine levels.
3. Immunology testing: Antiglomerular basement membrane antibodies, complement levels,
autoantibodies.
4. Kidney biopsy: Cause, the amount of scarring and potential for reversibility.
5.  Computed tomography (CT) scan, kidney ultrasound, chest X-ray.
Treatment:
•Causative disorder: Prompt treatment of underlying infection (eg, staphylococcal
endocarditis, malaria, syphilis, schistosomiasis)
•  Diuretics: fluid overload
• Treatment for high blood pressure: Diuretics, Angiotensin-converting enzyme (ACE)
inhibitors, Angiotensin II receptor blockers.
• Restricting the amount of protein in the diet is modestly helpful in reducing the rate of
kidney deterioration
• Restriction of sodium intake are considered beneficial.
• End-stage kidney failure can be treated with dialysis or a kidney transplant.
Prognosis:
• Acute poststreptococcal glomerulonephritis resolves completely in most cases,
especially in children.
• About 1% of children and 10% of adults develop chronic kidney disease.

• In some children and adults who do not recover completely from acute
glomerulonephritis, other types of kidney disorders develop, such as asymptomatic
proteinuria and hematuria syndrome or nephrotic syndrome.

• Other people with acute glomerulonephritis, especially older adults, often develop
chronic glomerulonephritis.

• If treatment occurs late, the person is more likely to develop chronic kidney disease
with kidney failure.

• Because kidney failure tends to develop before people notice it, 80 to 90% of people
who have rapidly progressive glomerulonephritis become dependent upon dialysis.

• The prognosis also depends on the cause, the person's age, and any other diseases the
person might have. When the cause is unknown or the person is older, the prognosis is
worse.
 Metabolism

In this phase urine is acidified due to H+ secretion by 3 different reactions;

1. H+ + HCO3- Carbonic H CO
anhydrase (CA) 2 3

2. H+ + NH3Cl NH4Cl

3. H+ + NaHPO4 NaH2PO4
 GFR influenced by:

• Blood pressure and blood flow

• Obstruction to urine outflow
• Loss of protein-free fluid
• Hormonal regulation
– Renin – angiotensin
– Aldosterone
– Antidiuretic Hormone (ADH)
– Atrial Natriuretic Peptide (ANP)