Transcript Selective Renal and GI conditions

Selective GI and Renal Conditions
Gastrointestinal Disorders
GERD
Gastritis
Peptic Ulcer Disease
Irritable Bowel Syndrome
GERD
• Gastroesophageal Reflux Disease
• Commonly known as ‘Heartburn’
Esophagus (1 of 3)
• Muscular tube that extends from pharynx to stomach
with sphincters at both upper and lower ends
– Upper sphincter relaxes to allow passage of swallowed food
– Lower (gastroesophageal or cardiac) sphincter relaxes to
allow passage of food to the stomach
• Diseases
– Failure of cardiac sphincter to function properly
– Tears in lining of esophagus from retching and vomiting
– At gastroesophageal junction from repetitive, intermittent,
vigorous contractions that increase intraabdominal pressure
– Esophageal obstruction from carcinoma, food impaction, or
stricture
Esophagus (2 of 3)
• Symptoms
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Difficulty swallowing (dysphagia)
Substernal discomfort or pain
Inability to swallow (complete obstruction)
Regurgitation of food into trachea
Choking and coughing
• Two major disturbances of cardiac sphincter
– 1. Cardiospasm: sphincter fails to open properly due to
malfunction of nerve plexus; esophagus becomes dilated
proximal to constricted sphincter from food retention
• Treatment: periodic stretching of sphincter; surgery
– 2. Incompetent cardiac sphincter: sphincter remains open;
gastric juices leak back into esophagus
Esophagus (3 of 3)
• Complications of incompetent cardiac sphincter
– Reflux esophagitis: inflammation
– Ulceration and scarring of squamous mucosal lining
– Barrett’s esophagus: glandular metaplasia; change from
squamous to columnar epithelium; ↑risk for cancer -a
disorder in which the lining of the esophagus is damaged by
stomach acid.
• Esophageal obstruction
– Carcinoma: can arise anywhere in esophagus
– Tumor narrows lumen of esophagus, infiltrates surrounding
tissue, invades trachea (tracheoesophageal fistula)
– Food impaction: distal part
– Stricture: from scar tissue due to necrosis and inflammation
from corrosive chemicals such as lye
Bolus of food
Tongue
Uvula
Pharynx
Bolus
Epiglottis
Epiglottis
Glottis
Trachea
Bolus
Esophagus
1 Upper esophageal sphincter is
contracted. During the buccal phase, the
tongue presses against the hard palate,
forcing the food bolus into the oropharynx
where the involuntary phase begins.
Relaxed muscles
2 The uvula and larynx rise to prevent food
from entering respiratory passageways. The
tongue blocks off the mouth. The upper
esophageal sphincter relaxes, allowing food
to enter the esophagus.
4 Food is moved
through the esophagus
to the stomach by
peristalsis.
Circular muscles
contract
Bolus of food
3 The constrictor muscles of the
pharynx contract, forcing food
into the esophagus inferiorly. The
upper esophageal sphincter
contracts (closes) after entry.
Relaxed
muscles
5 The gastroesophageal
sphincter opens, and food
enters the stomach.
Longitudinal muscles
contract
Gastroesophageal
sphincter closed
Gastroesophageal
sphincter opens
Stomach
Figure 23.13
Relaxed muscles
Circular muscles
contract
4 Food is moved through
the esophagus to the
stomach by peristalsis.
Bolus of food
Longitudinal muscles
contract
Gastroesophageal
sphincter closed
Stomach
Figure 23.13, step 4
Gastric mucosal tear caused by retching and
vomiting
Mallory–Weiss syndrome or gastro-esophageal
laceration syndrome refers to bleeding from tears (a
Mallory-Weiss tear) in the mucosa at the junction of
the stomach and esophagus, usually caused by
severe retching, coughing, or vomiting.
Gastritis
Acute Gastritis
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Inflammation of the gastric lining
Self-limited inflammation of short duration
May be associated with mucosal ulceration or bleeding
From nonsteroidal anti-inflammatory drugs (NSAID) that
inhibit cyclooxygenase (COX) enzyme: aspirin, ibuprofen,
naproxen
– COX-1: promotes synthesis of prostaglandin that protects
gastric mucosa
– COX-2: promotes synthesis of prostaglandin that mediate
inflammation
• Drugs that selectively inhibit COX-2 increase risk for heart attack and
stroke
• Alcohol: a gastric irritant; stimulates gastric acid
secretion
Surface
epithelium
Mucosa
Lamina propria
Submucosa
(contains submucosal
plexus)
Muscularis externa
(contains myenteric
plexus)
Serosa
Muscularis
mucosae
Oblique layer
Circular layer
Longitudinal
layer
(a) Layers of the stomach wall (l.s.)
Stomach wall
Figure 23.15a
Pepsinogen
HCl
Pepsin
Mitochondria
Parietal cell
Chief cell
Enteroendocrine
cell
(c) Location of the HCl-producing parietal cells and
pepsin-secreting chief cells in a gastric gland
Figure 23.15c
Blood
capillary
Chief cell
CO2
CO2 + H2O
Carbonic
H2CO3 anhydrase
H+
K+
Stomach lumen
H+-K+
ATPase
H+
K+
HCO3–
Alkaline
tide
HCI
Parietal cell
HCO3–
Cl–
Cl–
HCO3–- Cl–
antiporter
Cll–
Interstitial
fluid
Figure 23.18
H. Pylori Gastritis (1 of 2)
• Small, curved, gram-negative organisms that colonize
surface of gastric mucosa
• Grow within layer of mucus covering epithelial cells
• Produce urease that decomposes urea, a product of
protein metabolism, into ammonia
• Ammonia neutralizes gastric acid allowing organisms
to flourish; organisms also produce enzymes that
break down mucus layer
H. Pylori Gastritis (2 of 2)
• Common infection that increases with age (50%
by age 50)
• Spreads via person-to-person through close
contact and fecal-oral route
• Increased risk of gastric carcinoma: intestinal
metaplasia
• Increased risk of malignant lymphoma (mucosaassociated lymphoid tissue, MALT)
Bacteria
Mucosa
layer of
stomach
(a) A gastric ulcer lesion
(b) H. pylori bacteria
Figure 23.16
Peptic Ulcer
Peptic Ulcer
• Pathogenesis
– Digestion of mucosa due to increased acid secretions and
digestive enzymes (gastric acid and pepsin)
– Helicobacter pylori injures mucosa directly or through
increased acid secretion by gastric mucosa
– Common sites: distal stomach or proximal duodenum
• Complications: hemorrhage, perforation, peritonitis,
obstruction from scarring
• Treatment
– Antacids: block acid secretion by gastric epithelial cells
– Antibiotic therapy: against H. pylori
– Surgery if medical therapy fails
Bacteria
Mucosa
layer of
stomach
(a) A gastric ulcer lesion
(b) H. pylori bacteria
Figure 23.16
Gastric ulcer, eroded a blood
vessel at base of ulcer causing
profuse bleeding
Large, chronic
duodenal ulcer
Irritable Bowel Syndrome
• Also known as spastic colitis or mucous colitis
• Episodes of crampy abdominal discomfort, loud gurgling
bowel sounds, and disturbed bowel function without
structural or biochemical abnormalities
• Alternating diarrhea and constipation
• Excessive mucus secreted by colonic mucosal glands
• Diagnosis: by exclusion
– Rule out pathogenic infections, food intolerance, and
inflammatory conditions
• Treatment
– Reduce emotional tension
– Improve intestinal motility
Renal Disorders
Glomerulonephritis
Nephrotic vs. Nephritic Syndrome
Urinary Tract Infection
Vesicourethral Reflux
Renal Stones
Stress Urinary Incontinence
Glomerulonephritis
• Inflammation of the glomeruli caused by antigenantibody reaction within the glomeruli
• Immune-complex glomerulonephritis
– Usually follows a beta-streptococcal infection
– Circulating antigen and antibody complexes are filtered by
glomeruli and incite inflammation
– Leukocytes release lysosomal enzymes that cause injury to the
glomeruli
– Occurs in SLE; immune complexes trapped in glomeruli
– Occurs in IgA nephropathy
• Anti-glomerular basement membrane (anti-GBM)
glomerulonephritis: autoantibodies attack glomerular
basement membrane
Nephrotic
versus Nephritic Syndrome
• Nephritic syndrome is a collection of signs (syndrome) associated
with disorders affecting the kidneys, more specifically glomerular
disorders. It's characterized by having small pores in the
podocytes of the glomerulus, large enough to permit proteins
(proteinuria) and red blood cells (hematuria) to pass into the
urine.
• By contrast, nephrotic syndrome is characterized by only proteins
(proteinuria) moving into the urine. Both nephritic syndrome and
nephrotic syndrome result in hypoalbuminemia due to protein
albumin moving from the blood to the urine.
Diabetic Nephropathy
Kimmelstiel-Wilson syndrome
• Complication of long-standing diabetes
• Nodular and diffuse thickening of glomerular
basement membranes (glomerulosclerosis), usually
with coexisting nephrosclerosis
• Manifestations
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Progressive impairment of renal function
Protein loss may lead to nephrotic syndrome
No specific treatment can arrest progression of disease
Progressive impairment of renal function may lead to
renal failure
Urinary Tract Infections (1 of 2)
• Very common; maybe acute or chronic
• Most infections are caused by gram-negative bacteria
• Organisms contaminate perianal and genital areas and
ascend urethra
• Conditions protective against infection
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Free urine flow
Large urine volume
Complete bladder emptying
Acid urine: most bacteria grow poorly in an acidic
environment
Urinary Tract Infections (2 of 2)
• Predisposing factors
– Any condition that impairs free drainage of urine
– Stagnation of urine favors bacterial growth
– Injury to mucosa by kidney stone disrupts protective
epithelium allowing bacteria to invade deeper tissue
– Introduction of catheter or instruments into bladder may
carry bacteria
Cystitis
• Affects only the bladder
– More common in women than men; shorter female urethra,
and, in young sexually active women, sexual intercourse
promotes transfer of bacteria from urethra to bladder
– Common in older men, because enlarged prostate interferes
with complete bladder emptying
• Clinical manifestations
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Burning pain on urination
Desire to urinate frequently
Urine contains many bacteria and leukocytes
Responds well to antibiotics
May spread upward into renal pelvis and kidneys
Urethra
Figure 25.18a, b
Pyelonephritis
• Involvement of upper urinary tract from
– Ascending infection from the bladder (ascending
pyelonephritis)
– Carried to the kidneys from the bloodstream (hematogenous
pyelonephritis)
• Clinical manifestations: similar with an acute infection
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Localized pain and tenderness over affected kidney
Responds well to antibiotics
Cystitis and pyelonephritis are frequently associated
Some cases become chronic and lead to kidney failure
Vesicoureteral Reflux
• Urine normally prevented from flowing back
into the ureters during urination
• Failure of mechanisms allows bladder urine to
reflux into ureter during voiding
– Predisposes to urinary tract infection
– Predisposes to pyelonephritis
Vesicoureteral reflux
Urinary Calculi (1 of 3)
• Stones may form anywhere in the urinary tract
• Predisposing factors
– High concentration of salts in urine saturates urine causing
salts to precipitate and form calculi
• Uric acid in gout
• Calcium salts in hyperparathyroidism
– Urinary tract infections reduce solubility of salts in urine;
clusters of bacteria are sites where urinary salts may
crystallize to form stone
– Urinary tract obstruction causes urine stagnation, promotes
stasis and infection, further increasing stone formation
Urinary Calculi (2 of 3)
• Staghorn calculus: urinary stones that increase in size
to form large branching structures that adopt to the
contour of the pelvis and calyces
• Small stones may pass through ureters causing renal
colic
• Some become impacted in the ureter and need to be
removed
• Manifestations
– Renal colic associated with passage of stone
– Obstruction of urinary tract causes hydronephrosishydroureter proximal to obstruction
Urinary Calculi (3 of 3)
• Treatment
– Cystoscopy: snares and removes stones lodged in
distal ureter
– Shock wave lithotripsy: stones lodged in proximal
ureter are broken into fragments that are readily
excreted
Stress Urinary Incontinence
• Involuntary loss of urine due to increases in intra-abdominal
pressure