1. Anatomy
    2. 1. Kidney
    2. Urether
    3. Urinary bladder
    4. Urethra
    5. Intravenous Urography or Excretory pyelography
  2. Physiology
    3. 6. Overview of Functional Anatomy of Kidney
    7. Glomerular filtration
    8. Tubular functions
    9. Micturition
    10. Renal Function Test
  3. Pathology
    4. 11. Renal failure
    12. Uremia and Azotemia
    13. Glomerular diseases
    14. Rapidly progressive (Crescentic) glomerulo-nephritis (RPGN)
    15. Diabetic nephropathy
    16. Acute Tubular Necrosis
    17. Pyelonephritis and Urinary tract infection
    18. Renal calculi or Nephrolithiasis
    19. Hydronephrosis
    20. Tumors of Kidney
    21. Urinary bladder
    22. Tumors of Urinary bladder
    23. Polycystic kidney disease (PKD)
  4. Pharmacology
    5. 24. Diuretics
    25. Antidiuretics
    26. Urinary tract infection (UTI)
    27. Electrolyte balance
    28. Nephrotoxic drugs
  5. Microbiology
    6. 29. Urinary Tract Infection (UTI)
    30. Escherichia coli
    31. Enterococcus fecalis
    32. Renal tuberculosis
    33. Post streptococcal glomerulonephritis
  6. Biochemistry
    7. 34. Renal functions and Electrolyte balance
    35. Renal function tests
    36. Metabolism of amino acids and Non-nitrogenous compounds
    37. Amino acid pool
    38. Urea cycle or Krebs-Henseleit or Ornithine cycle
    39. Creatine metabolism
    40. Metabolic aspects of malignant diseases
    41. Water, Sodium and Potassium
Pharmacology
24. Diuretics
Image 11️⃣PCT2️⃣Loop of Henle3️⃣Thick Asceding Limb4️⃣DCT5️⃣Late DCT & Collecting tubule
RAS DRUGS
graph TD A(Angiotensinogen - Liver) -->|Low Blood pressure <br> Decrease renal perfusion pressure <br> <b>Renin</b> produced by juxtraglomerular cells of kidney| B(Angiotensin I) B -->|ACE - Lung🫁| C(Angiotensin II) C -->|AT1 receptor| D(Heart🫀) & E(Blood vessels🩸) & F(Kidney🫘) & G(Adrenal gland) & H(Brain🧠) & I(Sympathetic nervous <br>system😱) subgraph Effect of Angiotensin II D --> D1(Increases force,<br> velocity, and <br>rate of heart) E --> E1(Causes vasoconstriction, <br>increases venous return, <br>and cardiac output) F --> F1(Increases absorption of Na<sup>+</sup>) G -->|Increases aldosterone <br>synthesis| G1(Increase Na<sup>+</sup> and<br> water reabsorption <br>and K<sup>+</sup> loss.) & G11(Vasoconstriction.) H --> H1(Activates thirst center) I --> I1(Activates sympathetic<br> activity) end D1 & E1 & F1 & G1 & G11 & H1 & I1 --> J(Increases Blood pressure) J-->K((Decreased <br>Renin <br>production)) X(Bradykinin)-->|ACE - Lung🫁| Y(Inactive peptide) X-->Z(Causes Vasodilation <br>and Cough) Y-->|❌|Z
Angiotensin - 2
Uses
Heart
Increases force, velocity and rate of heart.
Blood vessels
Causes vasoconstriction and thus increases both Venous return and Cardiac output.
Kidney
Increases absorption of Na+.
Adrenal gland
Increases aldosterone synthesis and thus increases the absorption of Na+ and causes vasoconstriction.
Brain
Activates thirst center
Sympathetic nervous system
Activates the sympathetic activity.
Direct renin inhibitor
Drugs
Aliskiren
Mechanism of action
Pharmacokinetics
Pharmacodynamics
Uses
Adverse effect
Contraindication
ACE inhibitor
Drugs
  1. Captopril
  2. Enalapril
  3. Fosinopril
  4. Lisinopril
  5. Perindopril
  6. Ramipril
Table: Comparative features of some ACE inhibitors
Captopril
Enalapril
Fosinopril
Lisinopril
Perindopril
Ramipril
Chemical nature
Sulfhydryl
Carboxyl
Phosphinate
Carboxyl
Carboxyl
Carboxyl
Activity status
Active
Prodrug
Prodrug
Active
Prodrug
Prodrug
Bioavailability (as active form)
70% (Max)
50%
30%
25% (Min)
30–50%
60%
Time to peak action
1 hr
4–6 hr
3–5 hr
6–8 hr
6 hr
3–6 hr
Elimination t½*
2 hr
11 hr
12 hr
12 hr
25–30 hr
8–18 hr
Mode of excretion
Renal
Renal
Renal/hepatic
Renal
Renal
Renal
Duration of action
6–12 hr
24 hr
24 hr
> 24 hr
> 24 hr
> 24 hr
Daily dose (mg)
25–150
2.5–40
10–40
5–40
2–8
1.25–10
*t½ including that of active metabolite
Note
  1. Captopril and Fosinopril are only other than carboxyl compound.
  2. Capropril is prototype drug.
  3. Only Fosinopril have (Renal + Hepatic) mode of excretion, others have only renal mode of excretion.
  4. Captopril and Lisinopril are only active drugs, others all being pro-drugs.
  5. Bioavailability is maximum for Captopril(70%) and minimun for Lisinopril(25%).
Mechanism of action
Inhibits Angiotensin Converting Enzyme(ACE) produced by lung and thus prevent conversion of Angiotensi-I into Angiotensin-II.
Pharmacokinetics
Pharmacodynamics
Uses
  1. Hypertension
  2. Congestive Heart Failure
  3. Myocardial infarction
  4. Prophylaxis in high cardiovascular risk
  5. Diabetic nephropathy
  6. Scleroderma crisis
Adverse effect
  1. Hypotension
    • •
      There is little dilatation of capacitance vessels --> Postural Hypotension is not problem.
    • •
      But because of faster action of Captopril an initial sharp fall in BP first dose hypotension may occur.
    • •
      So start with ½ dose for 1 week before giving full dose.
  2. Foetopathic/ Teratogenic
    • •
      Use during second or third trimester may reduce fetal blood pressure leading to growth retardatioin, anuria and death.
  3. Hyperkalamia
    • •
      It is caused due to decrease aldosterone section. So more retention of potassium.
  4. Acute Renal Failure
  5. Cough
    • •
      It is caused due to suppression of ACE which results in inability to covert Bradykinin into Inactive peptide.
  6. Angioneurotic oedema
  7. Itch (Rashes, Urticaria)
  8. Dysgeusia
  9. Headache, Dizziness, Nausea and Bowel upset
Contraindication
  1. Pregnancy
  2. Allergy or Hypersensitivity
  3. Bilateral Renal artery stenosis
  4. Hyperkalamia
AT1 receptor blocker
Drugs
  1. Candesartan
  2. Losartan
  3. Irbesartan
  4. Olmesartan
  5. Telmisartan
  6. Valsartan
Mechanism of action
Blocks AT1 receptor present on different organs and inhibts its effect.
Pharmacokinetics
Pharmacodynamics
Uses
Adverse effect
Contraindication