How Body Fluids Maintain Homeostasis

Renal Mechanism / Long-Term Regulation of Blood Pressure

1. Renin–Angiotensin–Aldosterone System (RAAS)
2. Action of Antidiuretic Hormone (ADH)

1. Renin–Angiotensin–Aldosterone System (RAAS)

Trigger

Step-by-Step Cascade

Blood pressure decreases
        ↓
Blood flow to kidney is decreased
        ↓
Juxtaglomerular (JG) cells in the kidney are stimulated
        ↓
JG cells release RENIN into the bloodstream
        ↓
Renin acts on Angiotensinogen (produced by liver)
        ↓
Angiotensinogen → Angiotensin I (Ang I)
        ↓  [Angiotensin-Converting Enzyme (ACE) — in lung capillaries]
Angiotensin I → Angiotensin II (Ang II)
        ↓                          ↓
Causes vasoconstriction     Stimulates ALDOSTERONE secretion
(↑ Total Peripheral         (from zona glomerulosa of adrenal gland)
 Resistance)                         ↓
                        Increases Na⁺ and water reabsorption
                        by the kidneys (↑ ECF volume)
        ↓_________________________________↓
              LEADS TO INCREASE IN BP

Key Points

2. Antidiuretic Hormone (ADH) Action

Trigger

Step-by-Step Cascade

Blood pressure (BP) decreases
        ↓
ADH is released from the POSTERIOR PITUITARY gland
        ↓
ADH acts on two receptor types:
  • V1 receptors (vascular smooth muscle) → Vasoconstriction → ↑ TPR
  • V2 receptors (renal collecting ducts) → ↑ water reabsorption → ↑ ECF volume
        ↓
Increases ECF volume AND causes vasoconstriction
        ↓
LEADING TO INCREASE IN BP

Key Points

• ADH is also called vasopressin because of its powerful vasoconstrictive effect
• V1 receptors → vasoconstriction of arterioles
• V2 receptors → water reabsorption in collecting ducts (↑ ECF volume)
• Increased ECF volume → increased blood volume → increased BP

RAAS Diagram (from Histology: A Text and Atlas)

Comparison: RAAS vs. ADH

Also Noted in Your Textbook (Hypothalamus — Neural Mechanism)

• Anterior hypothalamus stimulation → vasoconstriction → ↑ BP
• Posterior hypothalamus stimulation → vasodilation → ↓ BP

Clinical Relevance

• ACE inhibitors (e.g., captopril, enalapril) block the conversion of Ang I → Ang II, reducing vasoconstriction and aldosterone secretion → used in hypertension and heart failure
• Angiotensin II receptor blockers (ARBs) (e.g., valsartan, losartan) block the action of Ang II at its receptor
• Aldosterone antagonists (e.g., spironolactone) block aldosterone's effect on Na⁺ reabsorption

Role of Decreased Plasma Osmolality in Homeostasis

What Causes Decreased Osmolality?

• A person drinks excess water
• Excessive IV fluids are given
• Solute loss exceeds water loss

How the Body Responds — Step-by-Step

Complete Cascade:

Person drinks water (excess H₂O)
        ↓
① Plasma osmolality DECREASES
  (solute amount same, but more water = dilution)
        ↓
② Osmoreceptors in the ANTERIOR HYPOTHALAMUS are INHIBITED
  (these receptors are exquisitely sensitive — respond to
   changes as small as 1 mOsm/L)
        ↓
③ Two simultaneous effects:
   A) THIRST is suppressed → ↓ water drinking behavior
   B) ADH secretion from POSTERIOR PITUITARY is INHIBITED
        ↓
④ Lower circulating ADH levels reach the kidneys
   → ↓ water permeability of principal cells in
     late distal tubule & collecting duct
        ↓
⑤a ↓ Water reabsorption by the collecting ducts
⑤b Excess water stays in tubule → excreted as urine
   → ↓ Urine osmolarity + ↑ Urine volume (dilute urine)
        ↓
⑥ Less water returned to circulation
   + Thirst suppressed (less drinking)
        ↓
Plasma osmolality rises back toward NORMAL (negative feedback)

Key Role: ADH is the Central Hormone

Where Does Decreased Osmolality Fit in the Previous Topic (BP Regulation)?

• ADH is released when BP decreases
• But if osmolality also decreases at the same time, it opposes ADH release
• The body must balance both signals:
  • ↓ BP → tries to stimulate ADH
  • ↓ Osmolality → tries to suppress ADH
• In general, severe hypotension can override osmolality signals and still trigger ADH release (volume/pressure takes priority over osmolality in emergencies)

Summary Table

TONSILS — Complete Notes

Definition

Waldeyer's Tonsillar Ring

Fig. 10.14 Tonsils — pharynx opened from posterior showing lymphoid tissue (green), plus histology of palatine and pharyngeal tonsils

Types of Tonsils — Individual Details

1. Pharyngeal Tonsil (Adenoids)

• Located on the roof of the nasopharynx, behind the choanae
• Shape: cauliflower-like
• Epithelium: pseudostratified ciliated columnar (respiratory) epithelium
• Has shallow infoldings (not deep crypts) between sagittally oriented mucosal elevations
• Clinical: In children, can enlarge (called adenoids/polyps) → obstructs choanae → mouth breathing, sinusitis, sleep disturbance, and if Eustachian tube is blocked → chronic ear infections

2. Palatine Tonsils

• Located in the tonsillar fossa (hollow between the palatine arches)
• Visible through the open mouth when the tongue is depressed
• Epithelium: stratified non-keratinized squamous epithelium
• Has 10–20 tonsillar crypts (deep invaginations)
• Contains aggregated lymphoid follicles with germinal centers
• Site of vigorous B lymphocyte proliferation → produces all immunoglobulin types
• Clinical:
  • Acute tonsillitis — bacterial infection → sore throat (angina) + dysphagia
  • Peritonsillar abscess — complication of acute tonsillitis
  • Tonsillolith — calcifications in crypts → halitosis, foreign body sensation
  • Mononucleosis — viral cause of tonsillar enlargement
  • Tonsillectomy — surgical removal (evidence suggests it may increase long-term autoimmune risk)

3. Lingual Tonsil

• Located on the base of tongue (posterior 1/3)
• Has bumpy surface with cryptlike infoldings surrounded by secondary nodules
• Mucous-secreting posterior lingual glands open at the base of crypts
• Clinical: Lingual tonsillar hypertrophy → sleep-disordered breathing, difficult intubation

4. Tubal Tonsil

• Located at the inner (pharyngeal) opening of the Eustachian tube
• Viewed as a continuation of the pharyngeal tonsil
• Clinical: Enlargement → obstructs Eustachian tube → hearing impairment, nasal speech, chronic ear infections

General Structure of Tonsils

• Secondary lymphoid follicles directly beneath mucosal epithelium
• Each follicle has:
  • Light-staining germinal center
  • Dark-staining lymphocyte halo (cap thickened toward epithelium)
• Crypts — deep infoldings that increase surface area for antigen exposure
• Lymphocyte diapedesis — lymphocytes and granulocytes migrate into the epithelium, making the epithelial boundary indistinct
• Enclosed by a tough fibrous capsule
• Efferent lymphatics drain into deeper cervical lymph nodes (no afferent lymphatics)

Development (Embryology)

• Palatine tonsils develop from the dorsal remnants of the lateral extension of the 2nd pharyngeal pouch
• Tonsillar crypts appear at ~12th week of gestation
• Capsule develops by 20th week
• Tonsillar pillars (palatoglossus and palatopharyngeus muscles) derive from the 2nd and 3rd pharyngeal arches

Blood Supply

Arterial Supply to Palatine Tonsil (5 arteries)

• The tonsillar branch of the facial artery is the major supply — penetrates the superior constrictor muscle to reach the tonsil

Venous Drainage

• Lingual and pharyngeal veins → drains into internal jugular vein

Nerve Supply & Lymphatic Drainage

• Nerve supply: Glossopharyngeal nerve (CN IX) and lesser palatine nerves
• Lymphatics: Drain to upper deep cervical lymph nodes (especially jugulodigastric node — the "tonsillar node")

Immunological Function

• Act as an "immunological early warning system" — encounter pathogens entering through mouth and nose
• Generate local immune responses via:
  • Proliferation of B lymphocytes → antibody production (all Ig types) + memory B cells
  • Generation of T helper and cytotoxic T cells
• Tonsils are part of MALT (Mucosa-Associated Lymphoid Tissue) — specifically the pharyngeal component

Summary Table